February 14, 2017 by Kevin Hattori Transmission electron micrograph (TEM) of Zika virus. Credit: Cynthia Goldsmith/Centers for Disease Control and Prevention

The protein that helps the sperm and egg fuse together in sexual reproduction can also fuse regular cells together. Recent findings by a team of biomedical researchers from the Technion-Israel Institute of Technology, Argentina, Uruguay and the U.S. show this protein is part of a larger family of proteins that helps other cells bind together to create larger organs, and which also allows viruses like Zika and Dengue to invade healthy cells.

For every sexually reproducing organism, sperm and egg fusion is the first step in the generation of a new individual. This process has been studied for more than 100 years in many organisms including humans, mice, insects, plants, sea urchins and even fungi. But the identity of the molecular machineries that mediate sperm and egg fusion remained unknown.

Now, the team led by Dr. Benjamin Podbilewicz, of the Technion Faculty of Biology, and Dr. Pablo S. Aguilar of Universidad Nacional de San Martin in Argentina, has demonstrated that the protein HAP2 a long known player in sperm-egg fusion is a protein that mediates a broad range of cell-cell fusion. Their findings were published recently in the Journal of Cell Biology.

HAP2 is found in plants, protists (e.g. algae, protozoa, and slime molds) and invertebrates, and is therefore considered an ancestral protein present at the origins of the first eukaryotic cells (cells with real nuclei). However, a closer look at HAP2 led the researchers to conclude that HAP2's roots are even older. Structural and phylogenetic analysis of HAP2 proteins revealed they are homologous to proteins used by viruses such as Zika and Dengue to fuse viral membrane to the membrane of the cell they invade.

According to the researchers, this means HAP2, FF and viral fusion proteins constitute a superfamily of membrane fusion proteins, which the authors named Fusexins (fusion proteins essential for sexual reproduction and exoplasmic merger of plasma membranes).

"Fusexins are fascinating machines that keep a structural core diversified to execute cell membrane fusion in very different contexts," says Prof. Podbilewicz. "Understanding the different structure-function relationships of fusexins will enable scientists to rationally manipulate cell-cell fusion in fertilization and tissue development. The added and very timely benefit is that it provides us greater understanding of how Zika and other viruses cause diseases in their target hosts."

The striking similarities between proteins that promote membrane fusion under very different contexts led the authors to dig into mechanistic details. Performing cell-cell fusion experiments, the researchers demonstrated that, like FF fusexins, HAP2 is needed in both fusing cells to promote membrane cell fusion. This bilateral requirement of HAP2 and FF fusexins differs from the viral mechanism of action, where fusexin is only present in the viral membrane (see figure).

The combined conservation of structure, sequence, and function imply that these proteins diverged from a common ancestor. Fusexins might have emerged 2-3 billion years ago to promote a primordial form of genetic material exchange between cells. Later, enveloped viruses took these fusion proteins to infect cells more efficiently. Finally, multicellular organisms adapted fusexins to sculpt organs like muscle and bone-repairing osteoclasts in vertebrates and skin and the vagina in worms through cell-cell fusion.

Explore further: Researchers Uncover Cell Fusion Mechanism

More information: Clari Valansi et al. HAP2/GCS1 is a gamete fusion protein homologous to somatic and viral fusogens, The Journal of Cell Biology (2017). DOI: 10.1083/jcb.201610093

Journal reference: Journal of Cell Biology

Provided by: Technion-Israel Institute of Technology

In a study that could shed light on disorders that occur in skeletal muscles, bone, the placenta, and other organs where fused cells are common, researchers at the Technion-Israel Institute of Technology and at the US National ...

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The protein that helps the sperm and egg fuse together in sexual reproduction can also fuse regular cells together. Recent findings by a team of biomedical researchers from the Technion-Israel Institute of Technology, Argentina, ...

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February 13, 2017 From left, normal and mutant maize plants. Credit: UC Riverside

How plant cells divide and how that contributes to plant growth has been one of the longstanding unsolved mysteries of cell biology. Two conflicting ideas have fueled the mystery.

The first idea is that cells divide merely to fill space in plant tissue, and therefore the orientation of the division is unimportant to growth. In other words, the contribution of individual cell behavior to overall growth isn't very important.

The second idea is that individual cells are the basic unit of life and their individual programs eventually build an organism. In other words, each new cell created contributes to proper patterning of the tissue. In this case, the orientation of each cell's division is critical for how the plant tissue is patterned and also impacts growth.

New findings by a University of California, Riverside-led team of researchers, lend support to the second idea, that the orientation of cell division is critical for overall plant growth. The work was just published in the journal Proceedings of the National Academy of Sciences.

The researchers, led by Carolyn Rasmussen, an assistant professor of plant cell biology at UC Riverside and Pablo Martinez, a graduate student working in Rasmussen's lab, together with Anding Luo and Anne Sylvester at University of Wyoming, were working with a maize mutant, called tangled1, with known defects in growth and division plane orientation of cells. Division plane orientation refers to the positioning of new cell walls during division.

They used time-lapse live cell imaging that represented hundreds of hours of maize, (commonly called corn in the United States), cells dividing. The time-lapse of imaging allowed them to characterize a previously unknown delay during cell division stages in the maize mutant. This study clarified the relationship between growth, timely division progression and proper division plane orientation.

This study suggests that delays during division do not necessarily cause growth defects, but that improper placement of new cell walls together with delays during division causes growth defects. Therefore, division plane orientation is a critical but potentially indirect factor for growth.

The findings might have long-term implications for increasing agricultural production. For example, during the Green Revolution of the mid-20th century, researchers developed short-stature, or dwarf, wheat and rice varieties that led to higher yields and are credited with saving over a billion people from starvation. Understanding the molecular mechanisms of plant growth might contribute in the long-term to developing more suitable short-stature maize varieties.

The paper is called "Proper division plane orientation and mitotic progression together allow normal growth of maize."

Explore further: How plant cells regulate growth shown for the first time

More information: Proper division plane orientation and mitotic progression together allow normal growth of maize, PNAS, http://www.pnas.org/cgi/doi/10.1073/pnas.1619252114

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How plant cells divide and how that contributes to plant growth has been one of the longstanding unsolved mysteries of cell biology. Two conflicting ideas have fueled the mystery.

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February 10, 2017 In a dividing cell (above), tiny organs called peroxisomes (green) are evenly distributed in distinctive arcs. In cells lacking the protein Pex11b, peroxisomes are no longer allotted equally. Credit: Laboratory of Mammalian Cell Biology and Development at The Rockefeller University/Science

When most cells divide, they simply make more of themselves. But stem cells, which are responsible for repairing or making new tissue, have a choice: They can generate more stem cells or differentiate into skin cells, liver cells, or virtually any of the body's specialized cell types.

As reported February 3 in Science, scientists at The Rockefeller University have discovered that this pivotal decision can hinge on whether or not tiny organ-like structures, organelles, are divvied up properly within the dividing stem cell.

"In order for the body's tissues to develop properly and maintain themselves, renewal and differentiation must be carefully balanced," says senior author Elaine Fuchs, the Rebecca C. Lancefield Professor and head of the Robin Chemers Neustein Laboratory of Mammalian Cell Biology and Development. "Our experiments suggest an unexpected role for the positioning and inheritance of cellular organelles, in this case enzyme-filled peroxisomes, in controlling this intricate balance."

An uneven division

The outer section of the skin, the epidermis, provides a protective barrier for the body, and stem cells reside deep within it. During development, these cells divide so that one renewing stem cell daughter remains inward while the other daughter differentiates and moves outward to become part of the epidermis' outer layers. First author Amma Asare, a graduate student in the lab, wanted to know how skin cells first emerge and begin this transition.

Looking in developing mouse skin, Asare devised an approach to identify genes that help guide the balance between new cells that either stay stem-like or differentiate. One particular protein, Pex11b, caught her attention. It is associated with the membrane that surrounds the peroxisome, an organelle that helps to free energy from food.

Asare showed that the protein seems to work by making sure the organelles are in the right locations so they can be divided between the daughter cells. In cells that lacked Pex11b, peroxisomes weren't divvied up evenlyin some cases, one daughter cell ended up with all of the peroxisomes and the other didn't get any at all. And for those cells whose peroxisome distribution was disrupted, cell division took longer, and the mitotic spindle, the structure that separates the daughters' genetic material, didn't align correctly.

The net result of depleting skin stem cells of Pex11b, Asare found, was that fewer daughter cells were able to differentiate into mature skin cells.

A delay changes fate

The researchers next moved peroxisomes around in the cell using a sophisticated laboratory technique, and the effect was the same. "If the peroxisomes are in the wrong positions during cell division, no matter how they get there, that slows down the process," Asare says.

The effect for the whole organism was dramatic: If peroxisome positioning was disrupted in the stem cells, the mice embryos could no longer form normal skin.

"While some evidence already suggested the distribution of organelles, including energy-producing mitochondria, can influence the outcome of cell division, we have shown for the first time that this phenomenon is essential to the proper behavior of stem cells and formation of the tissue," says Fuchs, who is also a Howard Hughes Medical Institute Investigator.

Explore further: Signals that make early stem cells identified

More information: Amma Asare et al, Coupling organelle inheritance with mitosis to balance growth and differentiation, Science (2017). DOI: 10.1126/science.aah4701

Journal reference: Science

Provided by: Rockefeller University

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Scientists discover an unexpected influence on dividing stem cells' fate - Phys.Org

As of now shes the only candidate in the race for Rochester mayor with an actual platform. Thats according to mayoral candidate Rachel Barnhart. On this edition of Need to Know, Barnhart talks problems, priorities, and plans for Rochester if elected.

Also on the show, hes a pioneering researcher in the intriguing and at times controversial world of stem cell biology and medicine. URMCs Mark Noble explains where the stem cell movement is heading and shares new discoveries you need to know about.

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February 9, 2017 The functions of Ror2 and IFT20 in invasive cancer cells. In healthy cells IFT20 regulates the formation and function of primary cilia. Many cancer cells lack cilia, and these cells induce and sustain the expression of IFT20 through the high expression of Ror2. IFT20 promotes the formation of Golgi-derived microtubules by binding with the GM130-AKAP450 complex in Golgi. By doing this it regulates the deployment of Golgi and transport of proteins within Golgi, both important parts of the formation of invadopodia. Credit: Kobe University

An international research team has discovered that the IFT20 protein helps some cancer cells to invade by facilitating the transportation of membranes and proteins within parts of the cell.

Primary cilia exist on the surface of almost all human cells, acting as "cell antenna" that receive information from outside the cell. IFT20 (intraflagellar transport 20) is a protein present in most human cells that plays an essential role in the formation and functions of these primary cilia. In healthy cells it acts as a "cargo adaptor" to transport proteins along microtubules within cilia, but many cells lose these cilia when they become cancerous. This research has shed light on the function of IFT20 in non-ciliated cancer cells for the first time. The discovery has potential applications for developing new cancer treatment methods that block invasive cancer cells by targeting IFT20. The findings were published on January 26 in the online edition of Scientific Reports.

This research was carried out by an international team including Associate Professor NISHITA Michiru (Kobe University Graduate School of Medicine Department of Physiology and Cell Biology), Professor MINAMI Yasuhiro (Kobe University Graduate School of Medicine, Department of Physiology and Cell Biology), Professor Victor W. Hsu (Harvard Medical School) and Professor Gregory J. Pazour (University of Massachusetts Medical School). Most cancer-related deaths are said to be caused by cell invasion and the consequent spread of cancer cells to other parts of the body (metastasis). To counter this, scientists are searching for the mechanism that controls the invasive properties of cancer cells.

Researchers already knew that a cell membrane protein known as Ror2 expresses highly in various cancer cells, and it promotes cancer cell invasion and metastasis. Professor Nishita's team investigated various kinds of non-ciliated cancer cells and discovered that Ror2 promoted cancer cell invasiveness by inducing the expression of IFT20.

Many tumor cells break through the barrier of the extracellular matrix and infiltrate their surroundings by forming protruding structures known as invadopodia (see figure). The formation of invadopodia requires membranes and proteins supplied by the intracellular transport system, using the Golgi complex. The Golgi complex must be close to invadopodia to deploy these materials. The team's findings demonstrate that in tumor cells, IFT20 induces the Golgi complex to form microtubules by promoting interaction between the Golgi proteins GM130 and AKAP450. It also regulates the structure of the Golgi complex and transport of proteins within the complex. "This research has clarified a new molecular mechanism related to the formation of Golgi-derived microtubules, and its important role in invasive cancer cells," said Professor Nishita.

The relationship between loss of cilia and a cell's cancerous properties remains unclear. IFT20 is involved in the formation and function of cilia in healthy cells, but in non-ciliated cancer cells it is now clear that IFT20 is responsible for the formation of invadopodia. By continuing to analyze the relationship between IFT20 and the loss of cilia, this line of research could help shed light on the fundamental question of why many cancer cells lack cilia. Additionally, if the specific regulatory mechanism of IFT20 in cancer cells is revealed, this knowledge could be used to develop treatment that targets IFT20 to block invasive cancer cells.

Explore further: Study reveals gene's role in male infertility

More information: Michiru Nishita et al, Ror2 signaling regulates Golgi structure and transport through IFT20 for tumor invasiveness, Scientific Reports (2017). DOI: 10.1038/s41598-016-0028-x

Journal reference: Scientific Reports

Provided by: Kobe University

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IFT20 protein's role in helping cancer cells to invade - Medical Xpress

Jonathan Singer, who helped build UC San Diego into a world leader in molecular and cell biology as one of the schools original biology faculty members, died Feb. 2 in La Jolla. He was 92.

Singer was on the chemistry faculty at Yale University when he was lured toUC San Diegoin 1961 by David Bonner, the founding chair of the universitys biology department.

Bonner believed that studying biology at the molecular level with chemistry as its basis would revolutionize the biological sciences and Singer, who had been mentored as a postdoctoral fellow by Nobel LaureateLinus Pauling, would be a perfect fit.

He was Bonners right-hand man and shared his vision of building a new kind of biology department focused on molecular approaches to all branches of the biological sciences, one that would be deeply interconnected by collaborative research, said Bill McGinnis, dean of the Division of Biological Sciences.

After Bonners death in 1964, Singer took over as the chair of the department and carried out much of his work, including planning the construction of the first building of the future School of Medicine.

In 1972, he and biochemist Garth Nicolson published a groundbreaking paper in Science on the Fluid Mosaic Model of the cell membrane, which would prove to explain a wide range of critical cellular processes, including cell-cell signaling, cell division, membrane budding and cell fusion.

In the last two decades of his life, Singer focused with colleague Nazneen Dewji on a novel approach to a treatment of Alzheimers disease that centered on the interaction between two cell membrane proteins beta-amyloid precursor protein and presenilin.

Singer was elected to the National Academy of Sciences in 1969 and the American Academy of Arts and Sciences in 1971, and hewon the E. B. Wilson Award from the American Society for Cell Biology in 1991.

He also was a University Professor of the University of California, an honor that has been awarded to only 41 members of the UC faculty.

He is survived by his daughter Julianne, son Matthew, niece Laura and nephew Bill, as well as granddaughter Grace and grandson Michael.

In lieu of flowers, the family requests that donations be made to the Alzheimers Association.

gary.warth@sduniontribune.com

Twitter: @GaryWarthUT

760-529-4939

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Jonathan Singer, original UCSD faculty member, dies at 92 - The San Diego Union-Tribune

The Chan Zuckerberg Biohub (CZ Biohub) said today it will commit more than $50 million to fund human disease research by its first cohort of 47 investigators from the faculty of the University of California, Berkeley, Stanford University, and the University of California, San Francisco (UCSF).

Each investigator will receive a five-year appointment and up to $1.5 million toward life science research in their areas of expertise. CZ Biohub said the investigators were selected from several academic departments at the three universities, including biology, chemistry, computer science, engineering, mathematics, and physics.

An international panel of 60 scientists and engineers evaluated more than 700 applications, the Biohub said.

CZ Biohub investigators share our vision of a planet without disease. To realize this vision, we are giving some of the worlds most creative and brilliant researchers access to groundbreaking technology and the freedom to pursue high-risk research, Joseph DeRisi, Ph.D., of UCSF, co-president of the Biohub, said in a statement.

CZ Biohub investigators will challenge traditional thinking in pursuit of radical discoveries that will make even the most stubborn and deadly diseases treatable, added Dr. DeRisi, who co-leads the Biohub with Stephen Quake, D.Phil., of Stanford University.

The investigators have agreed to make their draft publications widely available through pre-print servers to ensure the rapid dissemination of research results, the Biohub said.

Open science will also be advanced, the Biohub added, through plans to establish share technology platforms where Bay Area scientists can further their research and advance efforts to fight disease.

In addition to its investigator program, the Biohub is pursuing large-scale collaborative projects that include an Infectious Disease Initiative and the Cell Atlas.

The Biohub says that its scientists and engineers will apply advanced technologies to fight against infectious diseases with research focused on four key areas: new detection technologies, new treatments, new ways to prevent infection, and new approaches to rapid response when new threats emerge.

Through the Cell Atlas project, the Biohub aims to build an international collaboration that will map the cell types of the human body. The map, which will be available to researchers worldwide, is intended to help researchers gain new insights into cell biology related to the causes of human disease, potentially leading to new therapies.

The Biohub was launched when Mark Zuckerberg and his wife, Priscilla Chan, M.D., set aside $600 million over 10 years toward a research center that will foster collaborations by professionals across multiple disciplines, including engineers, computer scientists, biologists, chemists, and other innovators.

The Biohub was one of two projects announced in September by the Chan Zuckerberg Initiative, named for the pediatrician and the Facebook founder, chairman, and CEO. The Initiative also committed $3 billion toward basic research over the next decade, with the audacious goal of curing, preventing, or managing all diseases by the end of the century.

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Chan Zuckerberg Biohub Awards $50M+ to 47 Investigators - Genetic Engineering & Biotechnology News

KANSAS CITY, KANSAS Eighteen undergraduate, graduate and postdoctoral students were honored for their scientific research presentations at the 15th annual Kansas IDeA (Institutional Development Awards) Network of Biomedical Research Excellence (K-INBRE) symposium last month in Manhattan, Kansas.

The annual symposium is part of the K-INBRE initiative to identify and recruit promising university students into careers in biomedical research in Kansas. Led by the University of Kansas Medical Center, 10 campuses in Kansas and Oklahoma participate in the collaborative network.

Developing and recruiting biomedical researchers in Kansas is a priority for the K-INBRE program, said Doug Wright, principal investigator for K-INBRE and professor and director of graduate studies in anatomy and cell biology at KU Medical Center. With this program we strive to keep the biosciences in Kansas growing and thriving.

Students work in research laboratories or in their communities alongside scientist mentors to develop research projects. These projects give students early hands-on experience in laboratory or field research practice to better inform their future career choices in the biosciences. Overall, more than 140 research posters were accepted for presentation at the symposium in a new digital poster format.

The annual K-INBRE Symposium brings together the network of students, faculty and staff from KU Medical Center, Emporia State University, Fort Hays State University, Haskell Indian Nations University, Kansas State University, Pittsburg State University, KU, Washburn University and Wichita State University as well as Langston University in Langston, Oklahoma.

The following students, listed by campus, received cash prizes for their oral and poster presentations:

University of Kansas Lawrence campus

University of Kansas Medical Center

Fort Hays State University

Kansas State University

Langston University, Langston Okla.

Washburn University

Wichita State University

K-INBRE is a multi-disciplinary network designed to inspire undergraduates to pursue careers in biomedical research, enhance research capacity through faculty development and retention and expand the biomedical research infrastructure connecting several academic institutions. More information about the program can be found at http://www.k-inbre.org.

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Kansas, Oklahoma students honored for research in biosciences - KU Today

Quorum Technologies, market and technology leaders in electron microscopy coating and cryogenic preparation products, report on how their PP3010T Cryo-SEM preparation system is being used in the preparation of hydrated whole cells to be imaged using electron cryotomography in the Jensen Laboratory located at HHMI Caltech.

Image of fission yeast Schizosaccharomyces pombe cells prepared for TEM - by Vitrobot freezing on Quantifoil grids and Quorum PP3010T transfer for FEI Versa FIB milling.

Alasdair McDowall is the EM Center Director in the Jensen Laboratory at the Howard Hughes Medical Institute located at Caltech. Headed by Professor Grant Jensen, the Lab uses Electron Cryotomography (ECT) to study the molecular architecture of microbial cells and HIV in their native state. The focus is on the fundamentals of microbial cell biology such as cell division, movement and secretion, as well as the structure of HIV at all stages of its lifecycle.

The lab opened its doors in 2002 and continues to push the boundaries of high resolution imaging today. However, the investigation of frozen hydrated whole cells (beam and vacuum sensitive materials) in the electron microscope chamber requires new solutions. The advances in techniques for the preparation of cells by Cryo Focused Ion Beam Milling for structural characterization have recently provided a new insight of these delicate cellular architectures.

Image of fission yeast Schizosaccharomyces pombe cells prepared for TEM - by Vitrobot freezing on Quantifoil grids and Quorum PP3010T transfer for FEI Versa FIB milling.

Cryo Focused Ion Beam milling (cryo FIB milling) is a cutting-edge method for thinning vitrified biological samples that allows access to intracellular regions of thick specimens (> 1 um) with unprecedented ease and structural preservation. It provides the ability to move beyond imaging only small bacterial cells with electron cryotomography (ECT) and will allow the exploration of eukaryotic cells, tissues and microbial biofilms to the same molecular resolution that the group has achieved with individual bacterial cells for the past decade.

In addition, the ability to thin individual bacterial cells before imaging, without perturbing their structure, will provide higher contrast and resolution when necessary, even within already thin bacterial cells. Furthermore, the addition of a cryo-stage to the existing FIB mill at Caltech will allow for further development of much needed methods for correlating fluorescence microscopy and electron tomography for the targeting and identification of specific structures deep within eukaryotic cells, bacteria and tissues.

Image of fission yeast Schizosaccharomyces pombe cells prepared for TEM - by Vitrobot freezing on Quantifoil grids and Quorum PP3010T transfer for FEI Versa FIB milling.

Dr McDowall uses the Quorum PP3010T cryo sample preparation system. This is a highly automated, easy-to-use, column-mounted, gas-cooled Cryo-SEM preparation system suitable for most makes and models of SEM, FE-SEM and FIB/SEM. The Jensen group uses their prep system with an FEI Versa scanning electron microscope.

Dr McDowall

To obtain full details of Cryo-SEM preparation systems and other products available from Quorum Technologies, please visit http://www.quorumtech.com.

Acknowledgements: Quorum Technologies thanks the following for sharing their research: Professors Grant Jensen & Julia Greer and Drs Matt Swuilius, Shrawan Mageswaran & Wei Zhao.

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Use of the Quorum Cryo-SEM preparation system in microbial cell biology with electron cryotomography at the Jensen ... - News-Medical.net

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Hearing loss affects millions of people around the world, and in around half of those cases the root cause is genetic. Now, medical researchers have been able to restore the hearing and balance in mice by inserting mutated genes into their bodies. Two papers published in the Nature Biotechnology journal describe the results.

"We demonstrate recovery of gene and protein expression, restoration of sensory cell function, rescue of complex auditory function and recovery of hearing and balance behaviour to near wild-type levels," otolaryngologists from the Harvard Medical School say in the research paper.

It says the work shows an "unprecedented recovery of inner ear function" and claims the "biological therapies to treat deafness may be suitable for translation to humans".

During the work, young mice were used to prove the method works. The mice had been artificially administered with Usher syndrome type IC, which in human children causes deafness, balance dysfunction, and blindness.

Most people born with type I and type II Usher syndrome suffer with severe to profound hearing loss as well as vision problems. Those with type III experience hearing loss later in life. The work from the Harvard medical academics focussed purely on the hearing loss aspect of the syndrome.

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To tackle the deafness, the research team injected a synthetic version of the adeno-associated virus - which has very little impact on humans - into the ears of mice. Within the virus was a normal copy of the mutated Ush1c gene, which causes deafness in the syndrome. It was the first time scientists have been able to find a virus that can enter the inner ear and deliver genes to the inner and outer hair cells needed for normal hearing ability.

"Delivery of a normal copy of the mutated gene, Ush1c, to the cochlea soon after the mice were born led to high levels of Ush1c protein in outer and inner hair cells, repair of damaged hair cell bundles, and a robust improvement in hearing and balance behaviour, enabling profoundly deaf mice to hear sounds at the level of whispers," a statement published alongside the research said.

"They can restore the hearing defect by the gene transfer," Andrew Forge an emeritus professor of auditory cell biology at University College London and author on the first Nature paper, tells WIRED.

Ruth Taylor, another UCL researcher involved in the work, tested the gene transfer method with human tissue. Using vestibular tissue the UCL academics were able to show the virus could transfer the gene to the human tissue in culture. "They did a lot of proof of concept in mice," Forge says. "The bit we did is the extra bit to show this could work in people."

He explains the work - and the field in general - is trying to answer one big question: "Can you manipulate the system to cure things that are wrong?"

Forge adds: "These kinds of therapies, if there is going to be a therapy, will be the way it is going to be working".

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Gene therapy allows 'deaf' mice to hear - Wired.co.uk