Category Archives: Cell Biology

Cell Biology

Immune-Onc Therapeutics Announces FDA Clearance of IND Application to Initiate First-In-Human Trial of IO-108, a Novel Antagonist Antibody Targeting…

PALO ALTO, Calif.--(BUSINESS WIRE)--Immune-Onc Therapeutics, Inc. (Immune-Onc), a clinical-stage cancer immunotherapy company developing novel biotherapeutics targeting immunosuppressive myeloid checkpoints, today announced that the U.S. Food and Drug Administration (FDA) has cleared the companys Investigational New Drug (IND) application for IO-108, a novel antagonist antibody targeting Leukocyte Immunoglobulin-Like Receptor B2 (LILRB2, also known as ILT4) for the treatment of solid tumors. Preclinical data presented at the 2020 Society for Immunotherapy of Cancers annual meeting demonstrate that IO-108 functions as a myeloid checkpoint inhibitor. IO-108 reprograms immune-suppressive myeloid cells toward a pro-inflammatory phenotype, leading to enhanced innate and adaptive anti-tumor immunity.

"The clearance of the IO-108 IND represents another major milestone for Immune-Onc as we progress our pipeline of novel myeloid checkpoint inhibitors targeting the LILRB family of immune inhibitory receptors, said Charlene Liao, Ph.D., chief executive officer of Immune-Onc. We are highly encouraged by the strength of the preclinical data of IO-108 and are pleased that our expertise in LILRB biology and translational sciences enables us to advance this asset into the clinic. We look forward to initiating the trial to further understand the role of LILRBs in cancer, and to test the potential of IO-108 in treating patients with advanced solid tumors.

The Phase 1, multicenter, dose-escalation study will consist of a monotherapy cohort and a combination therapy cohort to evaluate the safety, tolerability, pharmacokinetics, and pharmacodynamics of IO-108 alone and in combination with pembrolizumab, an anti-PD-1 antibody. Biomarkers will be assessed to enable a mechanistic understanding of clinical data and inform future trials. This study may also provide an opportunity to identify preliminary efficacy signals. After determination of the recommended Phase 2 dose, Immune-Onc plans to evaluate the efficacy, safety, and tolerability of IO-108 in combination with pembrolizumab and as monotherapy in indication-specific expansion cohorts.

IO-108 binds to LILRB2 with high affinity and specificity and blocks the interaction of LILRB2 with multiple ligands that are involved in cancer-associated immune suppression including HLA-G, ANGPTLs, SEMA4A, and CD1d. In preclinical studies, treatment of various primary human immune cell systems containing myeloid cells with IO-108 results in enhanced pro-inflammatory responses to multiple stimuli that are relevant to anti-tumor immunity. As a single agent, IO-108 reverses the anti-inflammatory myeloid cell phenotype that results from tumor conditioning and promotes the differentiation of monocytes into pro-inflammatory dendritic cells. Moreover, IO-108 potentiates the effect of PD-1 blocking antibodies on CD4+ T cell activation in co-cultures with allogeneic macrophages. In mouse models IO-108 inhibits the growth of solid tumors, which is associated with enhanced T cell responses. Together these data demonstrate that IO-108 has the potential to provide additive or synergistic benefit in combination with standard-of-care immunotherapies and/or immunogenic therapies for solid tumors that are both resistant and sensitive to T-cell checkpoint inhibitors.

ABOUT LILRB2 (ILT4)

LILRB2, also known as ILT4, is expressed mostly on myeloid cells, including monocytes, dendritic cells, macrophages, and neutrophils. In solid tumors, interaction of LILRB2 with tumor microenvironment (TME) relevant ligands, including HLA-G, ANGPTLs, SEMA4A, and CD1d, makes myeloid cells pro-tumorigenic (tolerating or promoting tumor growth) and promotes tumor immune evasion.

ABOUT IMMUNE-ONC THERAPEUTICS, INC.

Immune-Onc Therapeutics, Inc. (Immune-Onc) is a clinical-stage cancer immunotherapy company dedicated to the discovery and development of novel myeloid checkpoint inhibitors for cancer patients. The company aims to translate unique scientific insights in myeloid cell biology and immune inhibitory receptors to discover and develop first-in-class biotherapeutics that disarm immune suppression in the tumor microenvironment.

Immune-Onc has a promising pipeline with a current focus on targeting the Leukocyte Immunoglobulin-Like Receptor subfamily B (LILRB) of myeloid checkpoints. Immune-Oncs focused platform approach has led to the development of several promising therapeutics across various stages of development, including IO-108 in Phase 1 clinical development for solid tumors and IO-202, a first-in-class antibody targeting LILRB4 (also known as ILT3), in Phase 1 clinical development for the treatment of acute myeloid leukemia (AML) and chronic myelomonocytic leukemia (CMML). The company also plans to evaluate IO-202 in solid tumors. The U.S. Food and Drug Administration granted IO-202 Orphan Drug Designation for treatment of AML in October 2020. Additional assets in Immune-Oncs pipeline include IO-106, a first-in-class anti-LAIR1 antibody, and multiple undisclosed programs for solid tumors and hematologic malignancies.

The company has strategic research collaborations with The University of Texas, Albert Einstein College of Medicine, and Memorial Sloan Kettering Cancer Center, and has invested in proprietary models, assays, and tools to interrogate the biology and translate this cutting-edge research into the development of novel therapies. Headquartered in Palo Alto, California, Immune-Onc has assembled a diverse team with deep expertise in drug development and proven track records of success at leading biotechnology companies. For more information, please visit http://www.immune-onc.com and follow us on Twitter and LinkedIn.

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Immune-Onc Therapeutics Announces FDA Clearance of IND Application to Initiate First-In-Human Trial of IO-108, a Novel Antagonist Antibody Targeting...

Cell Biology

UPMC-Pitt Researchers Receive Grant to Advance Liver Organoids – UPMC & Pitt Health Sciences News Blog – UPMC

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Researchers from the University of Pittsburgh Liver Research Center, McGowan Institute for Regenerative Medicine and Carnegie Mellon Universitys (CMU) Computational Biology Department have been awarded almost $1.5 million from the National Science Foundation (NSF) to develop new approaches for producing liver organoids tiny, lab-grown human organs that have potential for disease modeling, drug discovery and transplantation.

Mouse models are often used for research on human diseases, but there is a gap between studies in cells and animals and translation to humans, said principal investigator Dr. Mo Ebrahimkhani, associate professor of pathology and bioengineering at Pitt and member of the Pittsburgh Liver Research Center and the McGowan Institute. Organoids help fill that gap because they can capture the complexity of our human organs and tissues.

Dr. Mo Ebrahimkhani

To grow these mini organs, researchers start with induced pluripotent stem cells (iPSCs), which are made from adult cells. iPSCs can turn into almost any cell type, and given the right signals at the right time, they can grow into complex 3D organoids of multiple tissue types.

Traditionally, organoid development is directed by adding a cocktail of chemicals at different times. But this trial-and-error approach is hard to optimize and can introduce variability among batches, hampering reproducibility and scalability of organoid production and making it difficult to compare findings across labs. Another problem is that development can stall, leaving cells with immature or abnormal characteristics or lacking blood vessels, which are important for transplantation applications.

These challenges prompted the NSFs call for research proposals that apply multidisciplinary approaches to understand processes of cellular differentiation during organ development and improve production of mature, functional cells or organoids.

Ebrahimkhani, in collaboration with Dr. Samira Kiani, co-principal investigator and associate professor of pathology at Pitt, and Dr. Ziv Bar-Joseph, professor of computational biology and machine learning who heads the Systems Biology Group at CMU, received funding to develop liver organoids that can be produced consistently and reliably. The researchers aim to program iPSCs with genetic instructions that guide cells to produce liver tissues with specified structure and function, rather than relying on external addition of growth factors.

We will develop programmable organoids with genetic circuits and switches, allowing them to sense the cell types and states, so they know when its the right time to turn on and turn off their programs, Ebrahimkhani explained.

The cells can be frozen, stored and shipped to different labs, he said. This will improve reproducibility, reliability and sharing of the science.

To generate genetic programs for liver organoids, the researchers aim to understand the processes that control organ development by combining two different tactics.

To improve lab-grown liver organoids, researchers will use computational analyses and genetic tools to understand and guide organ development. Credit: Emma Br

Our lab uses synthetic biology to manipulate genetic pathways in cells. By building these pathways, we understand the process, said Ebrahimkhani. Its like building a car from all the individual components. As I build the car, I understand how it functions.

Bar-Josephs lab will use computational analyses to reconstruct models that help explain how cells differentiate and interact with one another during organ development, an approach termed systems biology.

Systems biology is like trying to understand the car by taking it apart and looking at its individual components, said Bar-Joseph. In this research, we aim to combine synthetic biology and systems biology to understand organ development.

As part of the grant, the researchers will also develop an outreach program to help educate the public about stem cell and organoid research. They will create videos and a website on the Tomorrow Life platform, a science communication filmmaking initiative directed by Kiani.

Although the grant will focus on liver organoids, the researchers say that their findings could also inform the development of other types of human organoids, such as brain, kidney or retina.

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UPMC-Pitt Researchers Receive Grant to Advance Liver Organoids - UPMC & Pitt Health Sciences News Blog - UPMC

Cell Biology

Dissecting the Unusual Biology of the SARS-CoV-2 Delta Variant – The Scientist

SARS-CoV-2 is fitter than ever. Its latest incarnation, the Delta (or B.1.617.2) variant, is the fastest-spreading form of the virus yet. First identified in India, which it swept through killing hundreds of thousands this spring, Delta has swiftly become the most dominant coronavirus variant worldwide. While its already driving rapid increases in hospitalizations and deathsoverwhelmingly in unvaccinated populationssimply by virtue of being more transmissible, it may also cause more severe disease than some previously dominating SARS-CoV-2 variants.

Meanwhile, emerging data suggest that when vaccinated people become infected with the Delta variant and develop symptomswhich, although increasing in frequency, remains exceedingly rare, officials reportthey might be as contagious as unvaccinated infected people. Those findings motivated the Centers for Disease Control and Prevention (CDC) to recommend in late July that in places with high transmission of the virus, even fully vaccinated people should wear masks indoors.

The Delta variants emergence isnt a shock to many researchers; spreading throughout the globe for a year and a half, SARS-CoV-2 was destined to adapt to humans and become better at infecting them. The mystery remains, however, exactly how Delta affects the human body differently than other variants. A flurry of recent research, little of which has undergone peer review, is yielding some clueson how the Delta variant might produce greater amounts of virus in peoples airways, for instance, which could make it more transmissible, and how it could cause more severe disease.

Scientists are also uncovering cause for hope. Although the antibodies induced by vaccines available in the US are slightly less effective against the Delta variant, the shots are largely still powerful protectors against severe cases of COVID-19. And according to preliminary data, breakthrough infections in vaccinated people resolve faster than in unvaccinated people.

Weve already seen a variety of other variants that have somebut maybe not allof the same characteristics that Delta has, such as increased transmission and a slight reduction in the effectiveness of vaccine-induced antibodies, says Richard Kennedy, an immunologist at the Mayo Clinic in Rochester, Minnesota. None of those are really a surprise. This [variant] just seems to have more of all of those.

Measuring SARS-CoV-2s transmissibility in the real world is notoriously difficult as human behavior is continuously changing, notes virologist Paul Bieniasz of Rockefeller University, but the fact that the Delta variant has so quickly displaced its dominating predecessor Alpha (B.1.1.7) is convincing evidence that its able to spread more rapidly in incompletely vaccinated populations. The UK governments Scientific Pandemic Influenza Group on Modelling, Operational sub-group (SPI-M-O) estimates that Delta is between 40 and 60 percent more transmissible than the Alpha variant and nearly twice as transmissible as the original virus first identified in China.

In explaining this heightened transmissibility, scientists point to not-yet-peer-reviewed data suggesting that infection with the Delta variant results in greater levels of virus accumulating more rapidly in human airways. In China, researchers tracked 62 people exposed to the virus who developed infections with the variant. They took daily measurements of the concentrations of viral RNA in swabs from the backs of the participants throats. Compared to 63 people infected with other variants, people with Delta infections tested positive sooner: four days after viral exposure compared to six. And when patients infected with Delta first tested positive, they carried around 1000 times more viral RNA. Although virologist Angela Rasmussen of the University of Saskatchewans Vaccine and Infectious Disease Organization cautions that viral RNA isnt necessarily a proxy for the amount of virus that is actually infectious, its probably a safe assumption that people are making more virus and shedding more virus when infected with the Delta variant, she says.

Perhaps the variant replicates faster inside cells or binds more tightly to human cells ACE2 receptor, which the viruss spike protein uses to enter cells, Kennedy speculates. But much attention has surrounded a particular mutation on the Delta variant called P681R, which suggests another potential mechanism. The mutation lies at the junction between two subunits of SARS-CoV-2s spike protein, at a site that allows the human cellular enzyme furin to cleave the spike into two parts. This cleavage, some experiments suggest, primes spike proteins in a way that allows them to fuse more readily with a host cells membrane, according to a detailed description in Nature.

The Delta variants P681R mutation seems to allow that cleavage to occur more efficiently than in the original SARS-CoV-2 strain. This could help the variant infect more cells in a given amount of time, and therefore, make more copies of itself overall. Having a more efficient furin cleavage site could lead to increased amounts of virus in the respiratory tract, Bieniasz says. The Alpha variantalso more transmissible than other versions of SARS-CoV-2 when it first emergedhas a similar mutation.

Some scientists are skeptical that the P681R mutation is to blame for the heightened viral load in people infected with Delta. Kei Sato, a virologist at the University of Tokyo, says that in his own experiments, he and his colleagues generally didnt observe much difference in replication or the ability to infect cells when comparing the Delta variant to a previously described form of the virus that lacks the P681R mutation. In any case, Bieniasz says hed be surprised if the Delta variants heightened transmissibility were caused by P681R alone. The variant carries a handful of other mutations on the spike protein, and more scattered around the genome. But there isnt really any information at this point that would tell you mechanistically what their contribution is to the increased fitness of Delta, he says.

The fact that the Delta variant has also triggered increasing numbers of infections in vaccinated people has generated a bevy of headlines, some of which have been criticizedfor their alarmist nature. The CDCs revised guidelines on mask-wearing were based in part on data from an outbreak in Massachusetts in the wake of large public gatherings. In July, officials identified 469 people in Barnstable County who tested positive, mostly for the Delta variant (participants had likely asked to be tested, and the majority had developed COVID-19 symptoms). Three-quarters were fully vaccinated, in part reflecting a relatively high vaccination rate in the area. Scientists stress that the vaccines still work as intended; they were designed to prevent severe disease, not infections. The Massachusetts study, for instance, reported only five hospitalizationsfour in fully vaccinated peopleand no deaths.

Nationwide, robust figures on the frequency of breakthrough cases are elusiveparticularly of asymptomatic or mild cases; the CDC only monitors instances that have progressed to hospitalization or death. According to an unpublished internal CDC document obtained by ABC News, breakthrough cases are reported for 0.096 percentor 153,000of the 156 million Americans who are fully vaccinated. A recent review of data from 25 states also estimated the rate of breakthrough cases to be well below 1 percent. According to that same review, the rates of hospitalizations and deaths with COVID-19 among the fully vaccinated range from effectively zero to 0.06 percent and 0.01, respectively.

Surprisingly, the Barnstable County study detected similar amounts of viral RNA in the specimens of vaccinated and unvaccinated participants. While thats not necessarily reflective of the peoples capacity to infect others, it is indisputable that in this outbreak, there seems to be transmission between previously vaccinated people, says Hana Akselrod, an infectious disease physician at George Washington University. The fact that participants had been gathering in bars and other crowed spaces probably created a high-risk setting for viral transmission, she adds.

Kennedy cautions that its hard to say how much of the increase in breakthrough infections is because of the Delta variants specific biology, rather than simply because its dominating a general surge in cases. But recent CDC data from Colorado does suggest vaccines are less effective against the variant; when it sped through Mesa County, the overall effectiveness of the available vaccines against symptomatic infection dropped to 78 percent, while in counties with lower Delta levels, it was 89 percent.

The variants fitness advantage could feasibly allow it to build up a high viral load before vaccinated immune systems crank out enough antibodies to quash it, Akselrod says. Anatomically speaking, its possible that while antibodies induced by current vaccines form high, protective levels in the lungswhere infection is associated with severe COVID-19 symptomsthey might be less able to access mucosal tissues in the nose and upper respiratory tract, allowing viral replication to occur there, Bieniasz speculates.

Another possible factor in establishing infections in vaccinated people is the Delta variants modest ability to evade vaccine-induced antibodies, Akselrod suggests. One yet-to-be-peer-reviewed paper posted to medRxiv in mid-July pitted antibodies isolated from 40 healthcare workers who had received either the Pfizer-BioNTech or Moderna mRNA vaccines against different variants. They found the Delta variant reduces the ability of antibodies to neutralize the virus by around 2.5-fold compared to a previously described isolateslightly more so than the Alpha variant but not as much as the Beta variant (B.1.351) first discovered in South Africa or the Gamma variant (P.1) first spotted in Brazil.

This is likely due to mutations to the Delta variants receptor binding domainthe patch on the spike protein that latches onto host cells ACE2 receptors and is targeted by vaccines, Kennedy says. What happens is the antibody either doesnt bind or doesnt bind as well, he explains. But the human immune system typically produces many different antibodies against individual viral proteinsnot to mention other kindsof immune machinerypreventing a complete reduction in vaccine effectiveness.

To wit: data from the Sisonke clinical trial in South Africa, reported in a news conference on Friday, suggest that even when it comes to Delta, the Johnson & Johnson vaccine is 71 percent effective against hospitalization and 95 percent effective against death. Rasmussen says she expects future variants to arise for which current vaccines are less protective, but for now, the vaccines are actually holding up very, very well against Delta.

In line with that idea is unpublished data from Singapore posted to medRxiv on July 31 that tracked Delta infections in 88 vaccinatedand mostly symptomaticpeople. Although their viral RNA loads for the first week of illness were similar to those recorded in a group of 130 infected unvaccinated people, they decreased much more quickly in the vaccinated group. And it showed that they had a huge spike in neutralizing antibodies immediately on testing positive, adds Rasmussen, who wasnt involved in the research.

Even so, several experts, including Rasmussen, Sato, and Bieniasz, agree with the CDCs recommendation that vaccinated people should wear masks in high-risk settings. No one wanted to be spending the summer sweating under masks, but this is the situation we have now, and we have to protect each other, Akselrod says. The primary use of masks is to prevent infections among unvaccinated people who are more contagious for longer and are most at risk for developing severe COVID-19 with Delta.

Its not clear if the elevated risk of hospitalization and death that someepidemiological studies have linked to Delta has more to do with characteristics of the populations in which Delta is circulating, or with the biology of the variant, Akselrod says. But some researchers have explored possible biological explanations. In a recent preprint, the University of Tokyos Sato and his colleagues report that when they allowed a SARS-CoV-2 isolate to infect modified monkey cells in vitro, the cells would stick together, forming connected structures known as syncytia, which have beenspotted in the lungs of people with COVID-19. The team suspected that SARS-CoV-2s furin cleavage site might be facilitating the observed clumping.

In addition to helping the viruses fuse with cells, its plausible that cleavage of the spike protein could also somehow cause infected cells to fuse with other cells close by. Notably, the team saw that syncytia induced by the Delta variantwhose P681R mutation may allow for more efficient cleavagewere much larger than those induced by a different form of SARS-CoV-2 that lacks the mutation. Interestingly, hamsters infected with SARS-CoV-2 viruses engineered to express the P681R mutation showed more signs of obstructed airways, and lost weight more quickly, than those infected with the other version of SARS-CoV-2suggesting the variant caused more severe disease. Sato hypothesizes that by causing larger syncytia to form, the Delta variant could be causing more severe tissue damage in the lung. I think that is the reason why the P681R-bearing virus is more pathogenic, he says.

Rasmussen isnt fully persuaded that the Delta variant is inherently more pathogenic. After all, hamsters are imperfect models of human COVID-19. But the P681R-driven syncytia formation might somehow explain why the virus is more transmissible, she says. Some other viruses are known to use such fused structures to spread from cell to cell, sometimes allowing more rapid spread across tissues.

Meanwhile, Akselrod says shes worried about a Delta-driven surge of mostly young, unvaccinated people wholl develop long-term symptoms known as long COVID. Amid a depleted healthcare workforce, the COVID-19 recovery clinic she directs is still struggling to care for long COVID patients who were infected with the Alpha variant in late 2020 or early 2021. To think of getting another giant wave of Delta on top of that is just very, very sad, she says. Its still unclear, though, whether long COVID may be proportionally more frequent with Delta, and whether even vaccinated people could develop long COVID. Thats a big scientific unknown right now, she says.

As researchers continue to chip away at questions about Delta, theyre also keeping in mind the new variants that are likely on the horizon. I think well see more variants that have increased transmissibility. We may or may not see variants that cause more severe disease. . . . Well undoubtedly see variants that have an increased ability to evade immune responses, Kennedy says. Well run out of letters in the Greek alphabet before we run out of variants.

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Dissecting the Unusual Biology of the SARS-CoV-2 Delta Variant - The Scientist

Cell Biology

Regenerative Medicine Market Size Worth $57.08 Billion By 2027: Grand View Research, Inc. – Markets Insider

SAN FRANCISCO, Aug. 12, 2021 /PRNewswire/ --The global regenerative medicine marketsize is expectedto reach USD 57.08 billion by 2027, growing at a CAGR of 11.27% over the forecast period, according to a new report by Grand View Research, Inc. Recent advancements in biological therapies have resulted in a gradual shift in preference toward personalized medicinal strategies over the conventional treatment approach. This has resulted in rising R&D activities in the regenerative medicine arena for the development of novel regenerative therapies.

Key Insights & Findings:

Read 273 page research report, "Regenerative Medicine Market Size, Share & Trends Analysis Report By Product (Cell-based Immunotherapies, Gene Therapies), By Therapeutic Category (Cardiovascular, Oncology), And Segment Forecasts, 2021 - 2027", by Grand View Research

Furthermore,advancements in cell biology, genomics research, and gene-editing technology are anticipated to fuel the growth of the industry. Stem cell-based regenerative therapies are in clinical trials, which may help restore damaged specialized cells in many serious and fatal diseases, such as cancer, Alzheimer's, neurodegenerative diseases, and spinal cord injuries. For instance, various research institutes have adopted Human Embryonic Stem Cells (hESCs) to develop a treatment for Age-related Macular Degeneration (AMD).

Constant advancements in molecular medicines have led to the development of gene-based therapy, which utilizes targeted delivery of DNA as a medicine to fight against various disorders. Gene therapy developments are high in oncology due to the rising prevalence and genetically driven pathophysiology of cancer. The steady commercial success of gene therapies is expected to accelerate the growth of the global market over the forecast period.

Grand View Research has segmented the global regenerative medicine market on the basis of product, therapeutic category, and region:

List of Key Players of Regenerative Medicine Market

Check out more studies related to Global Biotechnology Industry, conducted by Grand View Research:

Gain access to Grand View Compass, our BI enabled intuitive market research database of 10,000+ reports

About Grand View Research

Grand View Research, U.S.-based market research and consulting company, provides syndicated as well as customized research reports and consulting services. Registered in California and headquartered in San Francisco, the company comprises over 425 analysts and consultants, adding more than 1200 market research reports to its vast database each year. These reports offer in-depth analysis on 46 industries across 25 major countries worldwide. With the help of an interactive market intelligence platform, Grand View Research helps Fortune 500 companies and renowned academic institutes understand the global and regional business environment and gauge the opportunities that lie ahead.

Contact:Sherry JamesCorporate Sales Specialist, USAGrand View Research, Inc.Phone: 1-415-349-0058Toll Free: 1-888-202-9519Email: sales@grandviewresearch.comWeb: https://www.grandviewresearch.comFollow Us: LinkedIn| Twitter

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Regenerative Medicine Market Size Worth $57.08 Billion By 2027: Grand View Research, Inc. - Markets Insider

Cell Biology

Rewiring cell division to make eggs and sperm | Penn Today – Penn Today

To create eggs and sperm, cells must rewire the process of cell division.

Mitosis, the common type of cell division that human bodies use to grow everything from organs to fingernails and to replace aging cells, produces two daughter cells with the same number of chromosomes and approximately the same DNA sequence as the original cell. Meiosis, the specialized cell division that makes egg and sperm in two rounds of cell division, creates four granddaughter cells with new variations in their DNA sequence and half as many chromosomes in each cell. Meiosis uses most of the same cellular machinery as mitosis to achieve this very different outcome; only a few key molecular players prompt the rewiring from one type of division to another.

One such key player is the protein Meikin, which is found exclusively in cells undergoing meiosis. New research from Penns Michael Lampson and Jun Ma, collaborating with Whitehead Institute Member Iain Cheeseman and graduate student Nolan Maier, demonstrates how Meikin is elegantly controlled and sheds light on how the protein acts to serve multiple roles during different stages of meiosis.

The findings, which appear in the journal Developmental Cell, reveal that Meikin is precisely cut in half midway through meiosis. Instead of this destroying the protein, one half of the molecule, known as C-Meikin, goes on to play a critical role as a previously hidden protein actor in meiosis.

It was a pleasure working together to understand how some of the specialized meiotic functions that are necessary for making healthy eggs and sperm are controlled, says Lampson, a professor of biology in the School of Arts & Sciences.

Cells have this fundamental process, mitosis, during which they have to divide chromosomes evenly or it will cause serious problems like cancer, so the system has to be very robust, Maier says. Whats incredible is that you can add one or two unique meiotic proteins like Meikin and dramatically change the whole system very quickly.

During both mitosis and meiosis, sister chromatidscopies of the same chromosomepair up to form the familiar X shape of a chromosome. In mitosis, each chromatideach half of the Xis connected to a sort of cellular fishing line ,and these lines reel the chromatids to opposite ends of the cell, where the two new cells are formed around them.

In the first round of division in meiosis, however, the sister chromatids stick together, and one whole X is reeled into each new cell. Meikin helps to achieve this different outcome by ensuring that, while the chromosomes are being unstuck from each other in preparation for being pulled apart, each pair of sister chromatids stays glued together in the right place. Meikin also helps ensure that certain cellular machinery on the sister chromatids is fused so that they will connect to the same line and be reeled together to the same side of the cell.

More specifically, when chromosomes are first paired up, they are glued together by adhesive molecules in three regions: the centromere, or center of the X, where Meikin localizes; the region around the center; and the arms of the X. In the first round of meiosis, Meikin helps to keep the glue in the region around the center intact so the sister chromatids will stick together. Simultaneously, Meikin helps prime the center region to be unglued, while a separate process unglues the arms. This ungluing allows the chromosomes to separate and be prepared for later stages of meiosis.

Cheeseman and Maier initially predicted that Meikins role ended after meiosis I, the first round of meiotic cell division. In meiosis II, the second round of cell division, the cells being created should end up with only one sister chromatid each, and so the chromatids must not be kept glued together. Maier found that near the end of meiosis I Meikin is cleaved in two by an enzyme called Separase, the same molecule that cleaves the adhesive molecules gluing together the chromosomes. At first, this cleavage seemed like the end of Meikin and the end of this story.

However, unexpectedly, the researchers found that cells lacking Meikin during the second half of meiosis do not divide properly, prompting them to take another look at what happens to Meikin after it gets cleaved. They found that Separase cleaves Meikin at a specific point--carving it with the precision of a surgeons scalpelto create C-Meikin, a previously unknown protein that turns out to be necessary for meiosis II. C-Meikin has many of the same properties as the intact Meikin molecule, but it is just different enough to take on a different role: helping to make sure that the chromosomes align properly before their final division.

Theres a lot of protein diversity in cells that you would never see if you dont go looking for it, if you only look at the DNA or RNA. In this case, Separase is creating a completely different protein variant of Meikin than can function differently in meiosis II, says Cheeseman, who is also a professor of biology at the Massachusetts Institute of Technology. Im very excited to see what we might discover about other hidden protein forms in cell division.

Answering the question of Meikins role and regulation throughout meiosis required a close collaboration and partnership between Maier and Lampson lab senior research scientist Ma, the Lampson lab being experts on studying meiosis using mouse models. Working with mouse oocytes, or immature egg cells, Ma was able to reveal the behaviors and critical contributions of Meikin cleavage in meiotic cells in mice. Both labs credit the close exchange with helping them to get a deeper understanding of how cells rewire for meiosis.

Once cells have completed these specialized meiotic divisions, the researchers found that it was critical for oocytes to fully eliminate Meikin. They determined that, after meiosis II, C-Meikin is degraded by another molecule, the anaphase-promoting complex or APC/Cthis time for good. With Meikin gone and the rewiring of cell division reversed, eggs and sperm are ready for mitosis; should they fuse and form an embryo, that is the next cell division they will undergo. The researchers note that the way Meikin is regulated by being broken downfirst into C-Meikin and then completelymay help cells to organize their timing during meiosis. Breaking apart a protein is an irreversible step that creates a clear demarcation between before and after in a multi-step process.

The researchers hope that by uncovering the intricacies of meiosis, they may shed light on what happens when the creation of eggs and sperm goes wrong and perhaps contribute to the understanding of infertility.

Written by Greta Friar

The study was supported by grants from The Harold G & Leila Y. Mathers Charitable Foundation, the National Science Foundation (Grant 2029868), a Pilot award from the Global Consortium for Reproductive Longevity and Equity, the National Institutes of Health (GM126930 and GM122475), and the Henry and Frances Keany Rickard Fund Fellowship from the MIT Office of Graduate Education.

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Rewiring cell division to make eggs and sperm | Penn Today - Penn Today

Cell Biology

Stem Cell Scientists Explore the Latent Regenerative Potential of the Inner Ear – SciTechDaily

The organ of Corti, the hearing organ of the inner ear, contains rows of sensory hearing cells (green) surrounded by supporting cells (blue). Credit: Image by Yassan Abdolazimi/Segil Lab/USC Stem Cell

Scientists from the USC Stem Cell laboratory of Neil Segil have identified a natural barrier to the regeneration of the inner ears sensory cells, which are lost in hearing and balance disorders. Overcoming this barrier may be a first step in returning inner ear cells to a newborn-like state thats primed for regeneration, as described in a new study published inDevelopmental Cell.

Permanent hearing loss affects more than 60 percent of the population that reaches retirement age, said Segil, who is a Professor in the Department of Stem Cell Biology and Regenerative Medicine, and the USC Tina and Rick Caruso Department of Otolaryngology Head and Neck Surgery. Our study suggests new gene engineering approaches that could be used to channel some of the same regenerative capability present in embryonic inner ear cells.

In the inner ear, the hearing organ, which is the cochlea, contains two major types of sensory cells: hair cells that have hair-like cellular projections that receive sound vibrations; and so-called supporting cells that play important structural and functional roles.

When the delicate hair cells incur damage from loud noises, certain prescription drugs, or other harmful agents, the resulting hearing loss is permanent in older mammals. However, for the first few days of life, lab mice retain an ability for supporting cells to transform into hair cells through a process known as transdifferentiation, allowing recovery from hearing loss. By one week of age, mice lose this regenerative capacityalso lost in humans, probably before birth.

Based on these observations, postdoctoral scholar Litao Tao, PhD, graduate student Haoze (Vincent) Yu, and their colleagues took a closer look at neonatal changes that cause supporting cells to lose their potential for transdifferentiation.

In supporting cells, the hundreds of genes that instruct transdifferentiation into hair cells are normally turned off. To turn genes on and off, the body relies on activating and repressive molecules that decorate the proteins known as histones.In response to these decorations known as epigenetic modifications, the histone proteins wrap the DNA into each cell nucleus, controlling which genes are turned on by being loosely wrapped and accessible, and which are turned off by being tightly wrapped and inaccessible. In this way, epigenetic modifications regulate gene activity and control the emergent properties of the genome.

In the supporting cells of the newborn mouse cochlea, the scientists found that hair cell genes were suppressed by both the lack of an activating molecule, H3K27ac, and the presence of the repressive molecule, H3K27me3.However, at the same time, in the newborn mouse supporting cells, the hair cell genes were kept primed to activate by the presence of yet a different histone decoration, H3K4me1.During transdifferentiation of a supporting cell to a hair cell, the presence of H3K4me1 is crucial to activate the correct genes for hair cell development.

Unfortunately with age, the supporting cells of the cochlea gradually lost H3K4me1, causing them to exit the primed state. However, if the scientists added a drug to prevent the loss of H3K4me1, the supporting cells remained temporarily primed for transdifferentiation. Likewise, supporting cells from the vestibular system, which naturally maintained H3K4me1, were still primed for transdifferentiation into adulthood.

Our study raises the possibility of using therapeutic drugs, gene editing, or other strategies to make epigenetic modifications that tap into the latent regenerative capacity of inner ear cells as a way to restore hearing, said Segil. Similar epigenetic modifications may also prove useful in other non-regenerating tissues, such as the retina, kidney, lung, and heart.

Reference: 30 July 2021, Developmental Cell.DOI: 10.1016/j.devcel.2021.07.003

Additional co-authors of the study include Juan Llamas, Talon Trecek, Xizi Wang, andZlatka Stojanovain the Segil Lab at USC, and Andrew K. Groves at Baylor College of Medicine.

Sixty percent of this project was supported by federal funding from the National Institute on Deafness and Other Communication Disorders (R01DC015829, R01DC014832, T32DC009975, F31DC017376). Additional funding came from the Hearing Restoration Project at the Hearing Health Foundation.

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Stem Cell Scientists Explore the Latent Regenerative Potential of the Inner Ear - SciTechDaily

Cell Biology

Astellas and Minovia Therapeutics Announce Strategic Collaboration for Novel Mitochondrial Cell Therapy Programs – Business Wire

TOKYO & HAIFA, Israel--(BUSINESS WIRE)--Minovia Therapeutics, Ltd. (CEO; Natalie Yivgi-Ohana, Ph.D., Minovia) and Astellas Pharma Inc. (TSE: 4503, President and CEO: Kenji Yasukawa, Ph.D., Astellas) today announced a worldwide strategic collaboration and license agreement for the research, development, and commercialization of novel cell therapy programs for diseases caused by mitochondrial dysfunction.

Through this strategic collaboration, Astellas and Minovia aim to accelerate the creation of allogeneic mitochondrial cell therapy programs. The two companies will jointly research cell therapy program candidates comprised of cells derived from Astellas proprietary genetically-engineered, induced pluripotent stem cells and augmented with Minovias proprietary MAT platform technology. The goal of these programs will be to treat diseases caused by mitochondrial dysfunction, through the transfer of healthy mitochondria to restore the patients tissues.

Minovia is a leading company in the field of mitochondrial cell therapy that utilizes mitochondrial transfer to deliver healthy mitochondria to a patients diseased cells. Minovia has a unique technology platform called Mitochondrial Augmentation Therapy (MAT), where the patients own cells are isolated, loaded with healthy mitochondria obtained from a healthy donor, and then re-infused back into the patient. Minovia is currently conducting research, development and clinical studies with MAT in mitochondrial diseases.

Astellas is engaged through its US subsidiary companies, Astellas Institute for Regenerative Medicine (AIRM) and Universal Cells Inc., to advance allogeneic, off-the-shelf, differentiated cell therapy programs derived from pluripotent stem cells1. The new collaboration with Minovia extends Astellas capabilities in mitochondrial biology, and follow its recent acquisition of Mitobridge, Inc. and Nanna Therapeutics Limited2,3.

We are excited and honored to collaborate with Astellas, stated Minovias Co-founder and Chief Executive Officer, Natalie Yivgi-Ohana, Ph.D. We share with Astellas both their passion for mitochondrial science and their commitment to patients in need of new therapies. As Minovia continues the development of Mitochondrial Augmentation Therapy, we believe this partnership is critical to accelerate the development of off-the-shelf, allogeneic cell therapy programs for the many patients living with mitochondrial diseases caused by mitochondrial dysfunction.

Naoki Okamura, Representative Director, Corporate Executive Vice President, Chief Strategy Officer and Chief Financial Officer, at Astellas said, "We, at Astellas, have positioned mitochondrial biology as one of the Primary Focuses of our research and development strategy to develop therapies for patients with unmet medical needs. One of the aspirations of this Primary Focus is to establish a mitochondrial cell therapy platform. Minovia is pioneering mitochondrial cell therapy and has unique technologies for enhancing delivery of healthy mitochondria to the patients cells. This strategic collaboration with Minovia will accelerate and expand our pipeline of treatment options for patients with diseases with underlying mitochodrial dysfunction.

Under the terms of the agreement, Minovia receives an upfront cash payment of $20M USD. Through the joint research program with Minovia, if Astellas develops and commercializes product candidates for diseases caused by mitochondrial dysfunction, Minovia is eligible to receive up to $420M USD per product in future development, regulatory and commercial milestone payments from Astellas.

*1: R&D Meeting (December 10, 2020). Available at: https://sw4503.swcms.net/ja/ir-library/ir-meetings/inframe/main/014/teaserItems1/07/linkList/0/link/RDmeeting2020_pre_jp.pdf *2: Astellas Corporate website Accelerating the discovery and development of novel drugs that target mitochondrial functions.. Available at: https://www.astellas.com/jp/en/stories/science/mitobridge *3: Astellas Corporate website Primary Focus - Mitochondria Biology. Available at: https://www.astellas.com/jp/en/partnering/primary-focus#Mitochondria-Biology

About MinoviaMinovia Therapeutics, Ltd. is a clinical stage company and the first to use a mitochondrial cell therapy approach with the hope of bringing life-changing therapies to patients living with mitochondrial diseases, through their proprietary Mitochondrial Augmentation Therapy (MAT) platform. Minovia has an on-going autologous cell therapy program in clinical development, utilizing MAT for the future potential treatment of primary and secondary mitochondrial diseases. For more information, please visit our website at https://www.minoviatx.com.

About AstellasAstellas Pharma Inc. is a pharmaceutical company conducting business in more than 70 countries around the world. We are promoting the Focus Area Approach that is designed to identify opportunities for the continuous creation of new drugs to address diseases with high unmet medical needs by focusing on Biology and Modality. Furthermore, we are also looking beyond our foundational Rx focus to create Rx+ healthcare solutions that combine our expertise and knowledge with cutting-edge technology in different fields of external partners. Through these efforts, Astellas stands on the forefront of healthcare change to turn innovative science into value for patients. For more information, please visit our website at https://www.astellas.com/en.

Cautionary NotesIn this press release, statements made with respect to current plans, estimates, strategies and beliefs and other statements that are not historical facts are forward-looking statements about the future performance of Astellas. These statements are based on managements current assumptions and beliefs in light of the information currently available to it and involve known and unknown risks and uncertainties. A number of factors could cause actual results to differ materially from those discussed in the forward-looking statements. Such factors include, but are not limited to: (i) changes in general economic conditions and in laws and regulations, relating to pharmaceutical markets, (ii) currency exchange rate fluctuations, (iii) delays in new product launches, (iv) the inability of Astellas to market existing and new products effectively, (v) the inability of Astellas to continue to effectively research and develop products accepted by customers in highly competitive markets, and (vi) infringements of Astellas intellectual property rights by third parties. Information about pharmaceutical products (including products currently in development) which is included in this press release is not intended to constitute an advertisement or medical advice.

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Astellas and Minovia Therapeutics Announce Strategic Collaboration for Novel Mitochondrial Cell Therapy Programs - Business Wire

Cell Biology

Growing demand for Cell Culture-based Vaccine to propel the global Cell Culture Market – BioSpace

In molecular and cellular biology, cell culture acts as a significant tool for biological research. Today, most biotechnology products are primarily reliant on the mass culturing of animal cell lines. Cell cultures have found applications in diverse areas and serve as a model system for numerous research efforts.

An increase in funding from the government for cell-based research is significantly triggering the growth of the global cell culture market. In addition to this, cell culture techniques are widely used as an alternative to current egg-based strategies for the development of cell-based vaccines. With an increase in communicable diseases and the risk of a pandemic, cell culture has potential applications in the development of viral vaccines. Thus, cell culture technology is been extensively used in the development of U.S-licensed vaccines such as vaccines against rubella, smallpox, chickenpox, hepatitis, rotavirus, and polio. All such factors coupled with the growing prevalence of chronic diseases leading to a surge in demand for monoclonal antibodies and growing use of single-use technologies are escalating the growth of the global market.

Growing demand for cell culture products including equipment, reagents, and cell culture medium from academic and research institutes is fuelling the growth of the market. Moreover, the growing demand for 3D cell culture, major players focusing to expand the business in untapped regions, and the launch of new cell cultures are strengthening the growth of the global market. In March 2021, Thermo Fisher Scientific announced launch of new Gibco Human Plasma-like Medium (HPLM). It mimics the metabolic profile of human plasma and is the first cell culture medium that is especially designed to enable the researchers to get a realistic view of cell growth in the human body. Furthermore, growing demand for Covid-19 vaccine due to the rapid spread of deadly coronavirus will generate ample opportunities for the growth of the global market during the forecast period.

The global cell culture market is segregated based on product, application, end-user, and region. The product segment is bifurcated into consumables and instruments. The application segment is divided into stem cell technology, tissue engineering & regenerative medicine, drug screening & development, cancer research, and others. The end-user comprises pharmaceutical & biotechnology companies, research institutes, and others.

Regionally, North America is estimated to dominate the global cell culture market during the forecast period. This is majorly due to increase in cell culture-based vaccine approvals, growing demand from research institutes, and the growing prevalence of chronic diseases. Asia Pacific is predicted to grow rapidly during the forecast period. This is attributed to the increase in government funding for research purpose and the growing demand for cell culture products.

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Thermo Fisher Scientific, Becton, Dickinson and Company, Lonza Group AG, Danaher Corporation, GE Healthcare, Merck KGaA, Sartorius AG, HiMedia Laboratories, Eppendorf, and Corning Incorporated are some of the prominent players that are operating in the global cell culture market.

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Growing demand for Cell Culture-based Vaccine to propel the global Cell Culture Market - BioSpace

Cell Biology

Researchers Find Molecular Switch That Regulates Fat Burning in Mice – Newswise

Newswise BOSTON Linked to serious health problems including cancer, diabetes and cardiovascular disease, obesity affects more than a third of adults in the United States. Presently, there are few safe and effective nonsurgical therapeutic interventions available to patients with obesity.

Now, a multi-disciplinary team of researchers has demonstrated that a metabolic regulatory molecule called Them1 prevents fat burning in cells by blocking access to their fuel source. Led by microscopy experts at Beth Israel Deaconess Medical Center (BIDMC) and metabolism experts at Weill Cornell Medicine and NewYork-Presbyterian, the study may contribute to the development of a new type of obesity treatment. The teams findings were published June 9 in Nature Communications.

To help explain how the protein Them1 turns off heat production, BIDMCs cell biology and microscopy expert, Susan Hagen, PhD, associate vice-chair for research in the Department of Surgery at BIDMC, and Yue Li, PhD, a postdoctoral researcher in her laboratory, used light and electron microscopy to observe Them1 in action in mouse brown fat cells grown in the laboratory.

Them1 is an interesting molecule, said Hagen. If you inhibit or block its expression, metabolism increases and that reduces body weight.

The experiments showed that when the cells are stimulated to burn fat, a chemical modification causes Them1 molecules to spread out, or diffuse, throughout the cell. This frees the cellular powerhouses called mitochondria to efficiently turn the cells fat stores into energy. But when the stimulation stops, Them1 molecules quickly reorganize into a structure called a biomolecular condensate. Situated between the mitochondria and the fats they use as fuel, the condensed Them1 molecules limit energy production.

It turned out to be so incredibly interesting, said Hagen, who is also director of Microscopy and Histology Core Facilities at BIDMC and associate professor of surgery at Harvard Medical School. We asked other microscopy experts whether they had ever seen anything like the unusual images we found in resting cells. Using very sophisticated electron microscopy techniques, we were able to show for the first time, as far as we know what the bimolecular condensate looks like in electron microscopy.

The study explains a new mechanism that regulates metabolism, said David Cohen, chief of the Division of Gastroenterology and Hepatology at Weill Cornell Medicine and NewYork-Presbyterian/Weill Cornell Medical Center and the Vincent Astor Distinguished Professor of Medicine at Weill Cornell Medicine. Them1 hacks the energy pipeline and cuts off the fuel supply to the energy-burning mitochondria. Humans also have brown fat and produce more Them1 in cold conditions, so the findings may have exciting implications for the treatment of obesity.

Cohen and Hagen, both members of the Harvard Digestive Diseases Center, have been collaborators since 1983. The current study supported in part by a five-year, multi-PI grant from the National Institutes of Health also included collaborators with expertise in structural biology from Emory University.

This was the most fun I have ever had in science in my life, Hagen added. Including multiple primary investigators with different expertise gives you the power of doing things that you could never do on your own.

Co-authors included Yue Li, Samaksh Goyal, Lay-Hong Ang, and Mahnoor Baqai of BIDMC; Norihiro Imai, Hayley T. Nichols, Tibor I. Krisko of Weill Cornell; Blaine R. Roberts, Matthew C. Tillman, Anne M. Roberts, and Eric A. Ortlund of Emory University.

This work was supported by the National Institutes of Health (R01 DK 103046, R01 DK0488730 and NIHT32DK007533), the Harvard Digestive Disease Center (P30 DK034854) and the National Institutes of Health shared-instrumentation grant program for the High Pressure Freezer (S10 OD019988-01), the Pinnacle Research Award from the AAASLD Foundation, Weill Cornell Department of Medicine Pre-Career Award, and an American Heart Association Postdoctoral Fellowship, and a Research Science Institute/Center for Excellence in Education Summer Research Fellowship.

The authors declare no competing interests.

About Beth Israel Deaconess Medical Center Beth Israel Deaconess Medical Center is a patient care, teaching, and research affiliate of Harvard Medical School and consistently ranks as a national leader among independent hospitals in National Institutes of Health funding. BIDMC is the official hospital of the Boston Red Sox. For more information, visitwww.bidmc.org.

Beth Israel Deaconess Medical Center is a part of Beth Israel Lahey Health, a health care system that brings together academic medical centers and teaching hospitals, community and specialty hospitals, more than 4,000 physicians and 35,000 employees in a shared mission to expand access to great care and advance the science and practice of medicine through groundbreaking research and education.

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Researchers Find Molecular Switch That Regulates Fat Burning in Mice - Newswise

Cell Biology

New study shines light on how plant cells perceive and respond to mechanical forces – News-Medical.net

Minuscule tunnels through the cell membrane help cells to perceive and respond to mechanical forces, such as pressure or touch. A new study in the journal Science is among the first to directly investigate what one type of these mechanosensitive ion channels is doing in the tip-growing cells in moss and pollen tubes of flowering plants, and how.

Biologists led by Elizabeth Haswell at Washington University in St. Louis discovered that so-called PIEZO channels are not found along the plasma membrane in plant cells as they are in animal cells.

Instead, they observed that PIEZO channels have retreated into the plant cell, an unexpected discovery. PIEZO channels are found deeper within the cell, in the membranes of vacuoles -- the large, intracellular organelles that help maintain cell turgor and fulfill a number of other roles in the plant cell.

PIEZO channels in plants play a dramatic and critical role in regulating the shape of the vacuole and how much membrane there is."

Elizabeth Haswell, Professor of Biology in Arts & Sciences and a Howard Hughes Medical Institute-Simons Faculty Scholar

"This is the first example of PIEZO channels involved in regulating organelle morphology," she said. "The data we present could lead to new lines of investigation for both plant and animal PIEZO homologs."

As the name suggests, mechanosensitive ion channels are paths, or tunnels, through cell membranes that respond to mechanical forces. Under certain forces a channel opens, allowing the flow of ions across the membrane.

In humans, PIEZO channels are essential for life; without them, cell development halts. They are recognized for their role in perceiving light touch, shear force and compressive force. Dysfunction in PIEZO channels has been linked to multiple human diseases.

PIEZO channels were first identified in plant genomes in 2010. After a decade of research on animal homologs, this new research shines a spotlight on plant cells and explores how they differ from animal cells. Other research teams have recently shown that PIEZO channels are involved in mechanical sensing in plant roots.

The researchers made their initial discoveries using the tip-growing cells of a somewhat atypical model plant, spreading earthmoss (Physcomitrium patens).

But the scientists were able to extend their findings beyond moss to cells from other distantly related plants, including in pollen tubes in a classic model, the flowering plant Arabidopsis thaliana.

"Mosses are one of the groups that comprise the bryophytes, which are the second largest land plant lineage," said Ivan Radin, a research scientist in the Haswell laboratory and first author of the new paper.

"When we can show that the same thing happens both in moss and a flowering plant, as we did here, the most likely conclusion is that the process is ancestral -- it's at least as old as the land plants are," Radin said, noting that land plants colonized Earth about a half a billion years ago.

Radin became the Haswell laboratory's de facto moss specialist with coaching from co-author Magdalena Bezanilla, a professor of biological sciences at Dartmouth University. Bezanilla previously worked with Washington University's Ralph Quatrano, emeritus dean and the Spencer T. Olin Professor Emeritus of Biology, who was an early adopter of moss.

"The more time passes, the more we love it," Radin said. "Moss proved to be an exceptionally good model."

As a next step in this research, scientists in the Haswell laboratory are now conducting additional experiments to show how external and internal forces directly affect PIEZO channels in moss cells.

"Plant PIEZO channels are likely to be controlled by membrane tension in plants the same way they are in animals," Haswell said. The scientists are also exploring the evolution of these channels in algae.

Now they know where PIEZO channels are found in the cell, Haswell and her team are poised to find out what these proteins are doing in the vacuoles.

"We are looking at how PIEZO channel activation results in membrane elaboration and how it is regulated," Haswell said. "We want to know how the localization evolved and what it does in other cell types. We plan to compare and contrast the structure and function with the animal channels and in organisms across the green lineage."

Source:

Journal reference:

Radin, B., et al. (2021) Plant PIEZO homologs modulate vacuole morphology during tip growth. Science. doi.org/10.1126/science.abe6310.

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New study shines light on how plant cells perceive and respond to mechanical forces - News-Medical.net