Cells within our bodies divide and change over time, with thousands of chemical reactions occurring within each cell daily. This makes it difficult for scientists to understand whats happening inside. Now, tiny nanostraws developed by Stanford researchers offer a method of sampling cell contents without disrupting its natural processes.

Nicholas Melosh, associate professor of materials science and engineering, developed a new, non-destructive system for sampling cells with nanoscale straws. The system could help uncover mysteries about how cells function. (Image credit: L.A. Cicero)

A problem with the current method of cell sampling, called lysing, is that it ruptures the cell. Once the cell is destroyed, it cant be sampled from again. This new sampling system relies on tiny tubes 600 times smaller than a strand of hair that allow researchers to sample a single cell at a time. The nanostraws penetrate a cells outer membrane, without damaging it, and draw out proteins and genetic material from the cells salty interior.

Its like a blood draw for the cell, said Nicholas Melosh, an associate professor of materials science and engineering and senior author on a paper describing the work published recently in Proceedings of the National Academy of Sciences.

The nanostraw sampling technique, according to Melosh, will significantly impact our understanding of cell development and could lead to much safer and effective medical therapies because the technique allows for long term, non-destructive monitoring.

What we hope to do, using this technology, is to watch as these cells change over time and be able to infer how different environmental conditions and chemical cocktails influence their development to help optimize the therapy process, Melosh said.

If researchers can fully understand how a cell works, then they can develop treatments that will address those processes directly. For example, in the case of stem cells, researchers are uncovering ways of growing entire, patient-specific organs. The trick is, scientists dont really know how stem cells develop.

For stem cells, we know that they can turn into many other cell types, but we do not know the evolution how do they go from stem cells to, say, cardiac cells? There is always a mystery. This sampling technique will give us a clearer idea of how its done, said Yuhong Cao, a graduate student and first author on the paper.

The sampling technique could also inform cancer treatments and answer questions about why some cancer cells are resistant to chemotherapy while others are not.

With chemotherapy, there are always cells that are resistant, said Cao. If we can follow the intercellular mechanism of the surviving cells, we can know, genetically, its response to the drug.

The sampling platform on which the nanostraws are grown is tiny about the size of a gumball. Its called the Nanostraw Extraction (NEX) sampling system, and it was designed to mimic biology itself.

In our bodies, cells are connected by a system of gates through which they send each other nutrients and molecules, like rooms in a house connected by doorways. These intercellular gates, called gap junctions, are what inspired Melosh six years ago, when he was trying to determine a non-destructive way of delivering substances, like DNA or medicines, inside cells. The new NEX sampling system is the reverse, observing whats happening within rather than delivering something new.

Its a super exciting time for nanotechnology, Melosh said. Were really getting to a scale where what we can make controllably is the same size as biological systems.

Building the NEX sampling system took years to perfect. Not only did Melosh and his team need to ensure cell sampling with this method was possible, they needed to see that the samples were actually a reliable measure of the cell content, and that samples, when taken over time, remained consistent.

When the team compared their cell samples from the NEX with cell samples taken by breaking the cells open, they found that 90 percent of the samples were congruous. Meloshs team also found that when they sampled from a group of cells day after day, certain molecules that should be present at constant levels remained the same, indicating that their sampling accurately reflected the cells interior.

With help from collaborators Sergiu P. Pasca, assistant professor of psychiatry and behavioral sciences, and Joseph Wu, professor of radiology, Melosh and co-workers tested the NEX sampling method not only with generic cell lines, but also with human heart tissue and brain cells grown from stem cells. In each case, the nanostraw sampling reflected the same cellular contents as lysing the cells.

The goal of developing this technology, according to Melosh, was to make an impact in medical biology by providing a platform that any lab could build. Only a few labs across the globe, so far, are employing nanostraws in cellular research, but Melosh expects that number to grow dramatically.

We want as many people to use this technology as possible, he said. Were trying to help advance science and technology to benefit mankind.

Melosh is also a professor in the photon science directorate at SLAC National Accelerator Laboratory, a member of Stanford Bio-X, the Child Health Research Institute, the Stanford Neurosciences Institute, Stanford ChEM-H and the Precourt Institute for Energy. Wu is also the Simon H. Stertzer, MD, Professor; he is director of the Stanford Cardiovascular Institute and a member of Stanford Bio-X, the Child Health Research Institute, Stanford ChEM-H and the Stanford Cancer Institute. Pasca is also a member of Stanford Bio-X, the Child Health Research Institute, the Stanford Neurosciences Institute and Stanford ChEM-H.

The work was funded by the National Institute of Standards and Technology, the Knut and Alice Wallenberg Foundation, the National Institutes of Health, Stanford Bio-X, the Progenitor Cell Biology Consortium, the National Institute of Mental Health, an MQ Fellow award, the Donald E. and Delia B. Baxter Foundation and the Child Health Research Institute.

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Stanford-developed nanostraws sample a cell's contents without damage - Stanford University News

February 21, 2017 at 2:28 AM

How we think and fall in love are controlled by lightning-fast electrochemical signals across synapses, the dynamic spaces between nerve cells. Until now, nobody knew that cancer cells can repurpose tools of neuronal communication to fuel aggressive tumor growth and spread.

UT Southwestern Medical Center researchers report those findings in two recent studies, one in the Proceedings of the National Academy of Sciences (PNAS) and the second in Developmental Cell.

"Many properties of aggressive cancer growth are driven by altered cell signaling," said Dr. Sandra Schmid, senior author of both papers and Chair of Cell Biology at UT Southwestern. "We found that cancer cells are taking a page from the neuron's signaling playbook to maintain certain beneficial signals and to squelch signals that would harm the cancer cells."

The two studies find that dynamin1 (Dyn1) - a protein once thought to be present only in nerve cells of the brain and spinal cord - is also found in aggressive cancer cells. In nerve cells, or neurons, Dyn1 helps sustain neural transmission by causing rapid endocytosis - the uptake of signaling molecules and receptors into the cell - and their recycling back to the cell surface. These processes ensure that the neurons keep healthy supplies at the ready to refire in rapid succession and also help to amplify or suppress important nerve signals as necessary, Dr. Schmid explained.

"This role is what the cancer cells have figured out. Aggressive cancer cells have usurped the mechanisms that neurons use for the rapid uptake and recycling of neural transmitters. Instead of neural transmitters, the cancer cells use Dyn1 for rapid uptake and recycling of EGF (epidermal growth factor) receptors. Mutations in EGF receptors are drivers of breast and lung cancers," she said of the Developmental Cell study.

In order to thrive, cancer cells must multiply faster than nearby noncancerous cells. EGF receptors help them do that, she explained.

Cancer cell survival is another factor in disease progression. In the PNAS study, the Schmid lab found that aggressive cancer cells appear to have adapted neuronal mechanisms to thwart a key cancer-killing pathway triggered by activating "death receptors" (DRs) on cancer cells. Specifically, aggressive cancer cells appear to have adapted ways to selectively activate Dyn1 to suppress DR signaling that usually leads to cancer cell death.

"It is amazing that the aggressive cancers use a signaling pathway to increase the activity of EGF and also turn on Dyn1 pathways to suppress cancer death - so you have this vicious circle," said Dr. Schmid, who holds the Cecil H. Green Distinguished Chair in Cellular and Molecular Biology.

She stressed that less aggressive cancers respond to forms of chemotherapy that repress EGF signaling and/or die in response to the TRAIL-DR pathway. However, aggressive lung and breast cancer cells have adapted ways to commandeer the neuronal mechanisms identified in these studies.

The hope is that this research will someday lead to improved strategies to fight the most aggressive cancers, she said. Currently, her laboratory is conducting research to identify Dyn1 inhibitors as potential anticancer drugs using a 280,000-compound library in a shared facility at UT Southwestern.

"Cancer is a disease of cell biology. To grow, spread, and survive, cancer cells modify normal cellular behavior to their advantage. They can't reinvent the underlying mechanisms, but can adapt them. In these studies, we find that some cancer cells repurpose tools that neurons use in order to get a competitive advantage over nearby normal cells," she said.

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February 21, 2017 What are they going to be? Hematopoietic stem cells under the microscope: New methods are helping the Helmholtz scientists to predict how they will develop. Credit: Helmholtz Zentrum Mnchen

Autonomous driving, automatic speech recognition, and the game Go: Deep Learning is generating more and more public awareness. Scientists at the Helmholtz Zentrum Mnchen and their partners at ETH Zurich and the Technical University of Munich (TUM) have now used it to determine the development of hematopoietic stem cells in advance. In 'Nature Methods' they describe how their software predicts the future cell type based on microscopy images.

Today, cell biology is no longer limited to static states but also attempts to understand the dynamic development of cell populations. One example is the generation of different types of blood cells from their precursors, the hematopoietic stem cells. "A hematopoietic stem cell's decision to become a certain cell type cannot be observed. At this time, it is only possible to verify the decision retrospectively with cell surface markers," explains Dr. Carsten Marr, head of the Quantitative Single Cell Dynamics Research Group at the Helmholtz Zentrum Mnchen's Institute of Computational Biology (ICB).

He and his team have now developed an algorithm that can predict the decision in advance. So-called Deep Learning is the key. "Deep Neural Networks play a major role in our method," says Marr. "Our algorithm classifies light microscopic images and videos of individual cells by comparing these data with past experience from the development of such cells. In this way, the algorithm 'learns' how certain cells behave."

Three generations earlier than standard methods

Specifically, the researchers examined hematopoietic stem cells that were filmed under the microscope in the lab of Timm Schroeder at ETH Zurich. Using the information on appearance and speed, the software was able to 'memorize' the corresponding behaviour patterns and then make its prediction. "Compared to conventional methods, such as fluorescent antibodies against certain surface proteins, we know how the cells will decide three cell generations earlier," reports ICB scientist Dr. Felix Buggenthin, joint first author of the study together with Dr. Florian Bttner.

But what is the benefit of this look into the future? As study leader Marr explains, "Since we now know which cells will develop in which way, we can isolate them earlier than before and examine how they differ at a molecular level. We want to use this information to understand how the choices are made for particular developmental traits."

In the future, the focus will expand beyond hematopoietic stem cells. "We are using Deep Learning for very different problems with sufficiently large data records," explains Prof. Dr. Dr. Fabian Theis, ICB director and holder of the Mathematical Modelling of Biological Systems Chair at the TUM, who led the study together with Carsten Marr. "For example, we use very similar algorithms to analyse disease-associated patterns in the genome and identify biomarkers in clinical cell screens."

Explore further: Enough is enoughstem cell factor Nanog knows when to slow down

More information: Buggenthin, F. et al. (2017): Prospective identification of hematopoietic lineage choice by deep learning. Nature Methods, DOI: 10.1038/nmeth.4182

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Deep learning predicts hematopoietic stem cell development - Phys.Org

February 16, 2017 Credit: National Research Council of Italy

An International Reserach Team coordinated by Igb-Cnr has discovered a key role of vitamins and amino acids in pluripotent stem cells. The research is published in Stem Cell Reports, and may provide new insights in cancer biology and regenerative medicine

Vitamins and amino acids play a key role in the regulation of epigenetic modifications involved in the progression of diseases such as cancer. The research may have future implications in cancer biology. The study was published in Stem Cell Reports.

"We found that two metabolites, vitamin C and the amino acid L-Proline, are important players in the control of stem cell behaviour. This study shows that pluripotent embryonic stem cells present in the earliest phases of development are pushed toward a more immature 'naive' state by vitamin C, while they are forced to acquire a 'primed' state in the presence of L-Proline. Thus, vitamin C and L-Proline exert opposite effects on embryonic stem cells, and this correlates with their ability to modify DNA (DNA methylation) without altering the sequence, but instead, the regulation of gene expression," explained researcher Gabriella Minchiotti.

Stem cells possess the unique ability to self-renew and differentiate into other cell types, which makes them extremely interesting in medical and biological research. "Embryonic stem cells are the most 'potent' (defined as pluripotent), meaning that they can give rise to all cell types of an organism, such as cardiomyocytes, neurons, bones, etc. Like normal stem cells, cancer stem cells can also self-renew and differentiate, and are believed to be responsible for tumor growth and therapy resistance."

This study provides an important contribution to the understanding of how metabolites regulate pluripotency and shape the epigenome in embryonic stem cells, which have been largely unexplored and recently gained great interest. This knowledge not only enhances our understanding of the biology of normal stem cells but may offer novel insights into cancer stem cell biology, identifying novel potential therapeutic targets.

Explore further: Gene "bookmarking" regulates the fate of stem cells

More information: Stem Cell Reports, dx.doi.org/10.1016/j.stemcr.2016.11.011

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For most college freshmen, working in a lab typically means following the step-by-step instructions of class assignments with the goal of performing a specific experiment to produce a predetermined result.

But a handful of Harvard freshmen got the chance to experience real lab work by exploring how altering genes in yeast affected the cells functions.

Created by postdoctoral fellow James Martenson and Vlad Denic, a professor of molecular and cellular biology, the Wintersession class was designed to give undergraduates an up-close-and-personal view of the research that takes place in Harvard labs, and the opportunities they have to take part.

Students often arent aware these opportunities exist, so we think of this as a gateway for freshmen interested in doing research, Martenson said. But we also wanted to emphasize some of the critical thinking skills we use every day as scientists, but which may not be emphasized as much in more traditional coursework.

Over the course of the multiday class, each student worked with genetically altered strains of yeast to perform a series of three experiments.

We chose yeast because its a classic model organism in biology, Martenson said. A lot of very important work has been done in yeast. In fact, much of what we know about basic cell biology weve learned from yeast.

Using their various strains, he said, students performed a series of experiments aimed at testing how genetic changes altered organelle function.

A critical part of cell biology, organelles are essentially compartments inside cells, and include everything from mitochondria which act as the cells power plants to nuclei, which contain genetic material.

One key question in cell biology is how organelle quality is maintained, because many organelles house toxic chemical environments, Martenson explained. You also need a way to ensure the organelles are healthy, and if they do get sick, they need to be identified and eliminated before they cause a problem for the rest of the cell.

To probe questions of organelle health, Martenson is focusing on an organelle called the peroxisome and students did the same.

We started with a list of genes we had reason to believe were important for peroxisome function and quality control, but which were uncharacterized, he said. We thought it would be interesting for students to be involved in something that were actually interested in studying, so their work could yield interesting results that could inform our research.

For the students who took part, the experience was invaluable.

I didnt have a lot of lab experience, and I felt this class was a good way to expose myself to it, said Dylan Rice. I feel like Ive learned a lot, and Ive really enjoyed it so far.

Though she had already worked in another lab, Irla Belli said the relaxed atmosphere of the class helped her learn that making mistakes is often a key part of research.

You learn a lot from them, she said. In this four-day span, Ive learned more than from all the labs I had in class. This has solidified my desire to pursue the Ph.D. part of an M.D./Ph.D, and even though its very serious science, its relaxing.

For Amanda DiMartini, the class was a chance for an in-depth look at a field shes considering as a concentration.

I did some research in high school, but it was relatively simple, she said. Im interested in concentrating in some area of biology and this was a chance to see if I want to continue doing research throughout college. I feel like, in this class, were learning to think scientifically, and to think critically, and how to do research at a higher level. I dont regret [this class] at all.

By Colleen Walsh, Harvard Staff Writer | February 16, 2017

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Lab opens doors for an undergrad experience - Harvard Gazette

Gunnar Ask

George Klein, with his wife, Eva, discovered foundational phenomena in cancer research. He showed that normal cells carry genes, now known as tumour suppressors, that prevent cancer. He also worked out how the immune system comes to recognize and eliminate cancer cells.

Klein, who died on 10 December at the age of 91, had a youth filled with daring and peril. From a HungarianJewish family, he escaped being sent to a Nazi labour camp and from Russian patrols during the Second World War. He began medical studies in Budapest at the end of the war. In 1947, against all odds, a well-connected colleague arranged for Klein and a few other students to visit universities in Sweden. He was offered a place in the laboratory of the renowned cell biologist Torbjrn Caspersson at the Karolinska Institute.

Klein risked a return to communist Hungary to marry Eva, a fellow medical student he had known for mere weeks, and brought her back with him. The necessary documents typically took months to assemble, but he and Eva acquired them over a single workday using persuasion, pluck and bribes. They completed their PhDs at the Karolinska and maintained research groups there until about a month before George's death.

In 1957, a chair was created for him in tumour biology, a research field that he had helped to establish. The department of tumour biology that ensued was international and influential. Most of today's leading cancer researchers who are over 50 have had some interaction with George and his department. Seven secretaries wrangled his large correspondence. He invented social media before the technology existed.

A seminal paper published in 1960 (G. Klein et al. Cancer Res. 20, 15611572; 1960) dissected the essential basis of modern tumour immunology. Before it, researchers thought that all cancers carried a common antigen that the immune system could recognize. The Kleins and their colleagues used a chemical carcinogen to induce tumours in mice, surgically removed these and immunized the animals with irradiated cells from their own tumours. Next, the group inoculated mice with viable cancer cells and demonstrated that the immune system would only reject cancerous cells if they came from the original tumour.

This clarified the field: the immune system could recognize and reject cancers, in a way that was specific to each individual. A year later, Klein's team wrote a paper showing the other side of the coin (H. O. Sjgren et al. Cancer Res. 21, 329337; 1961). Tumours caused by the mouse polyomavirus do indeed share a common antigen. This paved the way for the general observation that tumours caused by or carrying viruses share common antigens that the immune system can target.

The Kleins' experimental success rested on two cornerstones. One was the establishment of a large colony of inbred mouse strains essential for tumour transplantation studies. After an early sabbatical at the Fox Chase Cancer Center in Philadelphia, George brought back 200 inbred mice on the return flight to found the colony.

The other was that the Kleins were among the first to apply concepts of population dynamics to cancer cells. This approach led to the demonstration of genes for tumour suppression (with their colleague at the Karolinska Francis Wiener and cell biologist Henry Harris) in the 1970s, at a time when it was not even clear that cancer had a genetic basis. This anticipated the modern view of cancer as resulting from the Darwinian evolution of cancer cells. Consecutive mutations in multiple genes increased the ability of wayward cells to survive, proliferate and evade checks against their growth.

Other seminal contributions included the prediction that translocations between chromosomes could activate oncogenes and the discovery of the Epstein-Barr virus nuclear proteins, which are crucial in the viral transformation of normal cells to a cancerous state. Their team (with Rolf Kiessling, then a graduate student at the Karolinska) also discovered, in 1975, natural killer cells, which can eliminate both cancerous and infected cells.

George showed an unusually high intellectual presence that mesmerized younger researchers. The tumour-biology department broke the boundaries of classic disciplines: it integrated genetics and mouse studies with cell biology, immunology and the study of infectious agents.

George also published books on the humanities, philosophy and popular science. Topics ranged from the Holocaust, atheism and religion to mysteries in cell biology and personal portraits of his heroes in science, music, poetry and literature. He was a leading public intellectual, often on Swedish television and in newspapers. His last book, Resistance (Albert Bonniers Frlag, 2015; published in Swedish), won the prestigious Gerard Bonnier prize for the best essay collection of that year. It deals with resistance to extremism and to cancer. Throughout his life, George was preoccupied with the thin borders between evil and good, and health and disease.

He was an admired lecturer for general and scientific audiences. His preferred format was conversation with an interesting opponent. There was a time when most major international cancer conferences concluded with his creative remarks. Many are those who can witness how much they were affected by bouncing ideas and results around with George.

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George Klein (19252016) - Nature.com

Live cell time-lapse imaging of maize mutant provides crucial details for UC Riverside researchers

By Sean Nealon on February 13, 2017

From left, normal and mutant maize plants.

RIVERSIDE, Calif. (www.ucr.edu) 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 isnt 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 cells 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 Rasmussens 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.

Scanning electron micrographs of maize epidermal cells. Left is the mutant variety. Right is the wild variety.

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.

Archived under: Science/Technology, Carolyn Rasmussen, College of Natural and Agricultural Sciences, Department of Botany and Plant Sciences, Pablo Martinez, press release

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Mutant Maize Offers Key to Understanding Plant Growth - UCR Today (press release)

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

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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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