Tag: Cellular Processes

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Scientists Shine Light on What Triggers REM Sleep

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Illustration of a brain.
While studying how the brain controls REM sleep, researchers focused on areas abbreviated LDT and PPT in the mouse brainstem. This illustration shows where these two areas are located in the human brain. Credit: Wikimedia Commons. View larger image

Has the “spring forward” time change left you feeling drowsy? While researchers can’t give you back your lost ZZZs, they are unraveling a long-standing mystery about sleep. Their work will advance the scientific understanding of the process and could improve ways to foster natural sleep patterns in people with sleep disorders.

Working at Massachusetts General Hospital and MIT, Christa Van Dort, Matthew Wilson, and Emery Brown focused on the stage of sleep known as REM. Our most vivid dreams occur during this period, as do rapid eye movements, for which the state is named. Many scientists also believe REM is crucial for learning and memory.

REM occurs several times throughout the night, interspersed with other sleep states collectively called non-REM sleep. Although REM is clearly necessary—it occurs in all land mammals and birds—researchers don’t really know why. They also don’t understand how the brain turns REM on and off.

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Zinc’s Role in Healthy Fertilization

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Fluorescent sensors at the cell surface show zinc-rich packages being released from the egg during fertilization. Credit: Northwestern Visualization.

Whether aiding in early growth and development, ensuring a healthy nervous system or guarding the body from illness, zinc plays an important role in the human body.

Husband-and-wife team, Thomas O’Halloran Exit icon and Teresa Woodruff, plus other researchers at Northwestern University, evaluated the role that zinc plays in healthy fertilization. The study revealed how mouse eggs gather and release billions of zinc atoms at once in events called zinc sparks. These fluxes in zinc concentration are essential in regulating the biochemical processes that facilitate the egg-to-embryo transition.

The scientists developed a series of techniques to determine the amount and location of zinc atoms during an egg cell’s maturation and fertilization as well as in the following two hours. Special imaging methods allowed the researchers to also visualize the movement of zinc sparks in three dimensions.

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Cells by the Numbers

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Cells are the basic unit of life—and the focus of much scientific study and classroom learning. Here are just a few of their fascinating facets.

3.8 billion

Nerve Cells
Developing nerve cells, with the nuclei shown in yellow. Credit: Torsten Wittmann, University of California, San Francisco.

That’s how many years ago scientists believe the first known cells originated on Earth. These were prokaryotes, single-celled organisms that do not have a nucleus or other internal structures called organelles. Bacteria are prokaryotes, while human cells are eukaryotes.

0.001 to 0.003

This is the diameter in centimeters of most animal cells, making them invisible to the naked eye. There are some exceptions, such as nerve cells that can stretch from our hips to our toes, sending electrical signals throughout the body.

1665

Red blood Cells
Oxygen-transporting red blood cells. Credit: Dennis Kunkel, Dennis Kunkel Microscopy, Inc.

In that year, British scientist Robert Hooke coined the term cell to describe the porous, grid-like structure he saw when viewing a thin slice of cork under a microscope. Today, scientists study cells using a variety of high-tech imaging equipment as well as rainbow-colored dyes and a green fluorescent protein derived from jellyfish.

200

That’s how many different types of cells are in the human body, including those in our skin, muscles, nerves, intestines, blood and bones.

3 to 5

Believe it or not, that’s the approximate number of pounds of bacteria you’re carrying around, depending on your size. Even though bacterial cells greatly outnumber ours, they’re much smaller than our cells and therefore account for less than 3 percent of our body mass. Scientists are learning more about how our body bacteria contribute to our health.

24

Snapshot of a phase of the cell cycle.
A snapshot of a phase of the cell cycle. Credit: Jean Cook and Ted Salmon, UNC School of Medicine.

This is the typical length in hours of the animal cell cycle, the time from a cell’s formation to when it splits in two to make more cells.

120

That’s the approximate lifespan in days of a human red blood cell. Other cell types have different lifespans, from a few weeks for some skin cells to as long as the life of the organism for healthy neurons.

50 to 70 billion

Each day, approximately this many cells die in the human body as part of a normal process that serves a healthy and protective role. Those that die in the largest numbers are skin cells, blood cells and some cells that line structures like organs and glands.

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Modifying Bacterial Behavior

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Biofilm
Communication through quorum sensing is key to the formation of biofilms, slimy bacterial communities that can cause infections and are often stubbornly resistant to antibiotics. Credit: P. Singh and E. Peter Greenberg.

Like a person trailing the aroma of perfume or cologne, bacteria emit chemical signals that let other bacteria of the same species know they’re there. Bacteria use this chemical communication system, called quorum sensing, to assess their own population size. When they sense a large enough group, or quorum, the microbes modify their behavior accordingly. Many disease-causing bacteria use quorum sensing to launch a coordinated attack when they’ve amassed in sufficient numbers to overwhelm the host’s immune response.

Chemist Helen Blackwell of the University of Wisconsin-Madison has been making artificial compounds that mimic natural quorum-sensing signals, as well as some that block a natural signal from binding to its protein target—a step needed to produce a change in bacterial behavior. By altering key building blocks in these protein targets one by one, Blackwell’s team found that small changes could convert an activation signal into an inhibitory signal, or vice versa, indicating that small-molecule control of quorum sensing is very finely tuned.

Improved understanding of the molecular basis of quorum sensing could help scientists design more potent compounds to disrupt these signals. Using such compounds to quiet quorum sensing may provide a new way to control disease-causing bacteria that reduces the chances an infection will become resistant to treatment.

This work was funded in part by NIH under grants R01GM109403 and T32GM008505.

Learn more:
University of Wisconsin-Madison News Release Exit icon
Blackwell Lab Exit icon

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Steering Cells Down the Right Path

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In these time-lapse videos (no longer available) of 60 images taken over an hour, cell receptors move around the cell surface in search of the missing signal that will tell the cell where to go (top video). Once the receptors locate the signal (bottom video), they stay put in the region of the cell membrane that is closest to the signal. Credit: David Sherwood, Duke University.

Even traveling cells need help with directions. In fact, it’s crucial. For processes such as wound healing and organ development to take place, cells must be able to efficiently move throughout organisms. Receptor proteins on a cell’s surface rely on navigational signals from molecules called netrins to point them in the right direction.

The receptors don’t just sit around waiting for a signal. Studying the simple worm C. elegans, David Sherwood Exit icon and his research team at Duke University discovered that in the absence of netrin, the receptors rapidly cluster and reassemble in different areas of the cell’s membrane. When the receptors finally detect a netrin signal, they stabilize and correctly orient the cell. The finding might point to new ways to interfere with cells’ built-in navigation systems to hamper cell migration in metastatic cancer or encourage the regrowth of damaged cells in neurodegenerative diseases such as Parkinson’s.

This research was funded in part by NIH under grants R01GM100083 and P40OD010440.

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Duke University News Release Exit icon

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Cool Image: Training Cells to Devour Dying Neighbors

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A healthy cell that has ingested dying cells.

A healthy cell (green) that has ingested dying cells (purple). Credit: Toru Komatsu, University of Tokyo.

In this image, a healthy cell (green) has engulfed a number of dying cells (purple) just as a predator might ingest wounded or dying prey. A team of researchers is hoping to use this same strategy at the cellular level to help treat infection, neurodegenerative diseases or cancer.

Our bodies routinely use a process called phagocytosis to rid themselves of unhealthy cells. Takanari Inoue at Johns Hopkins University and collaborators at the University of Tokyo set out to investigate the molecular underpinnings of phagocytosis. Their goal was to endow laboratory-grown human cells with phagocytotic skills, namely the ability to recognize, swallow and digest dying cells. The scientists tried to do this by inserting into the cells two molecules known to play a role in phagocytosis.

The engineered cells accomplished the first two tasks—they recognized and surrounded dying cells. But they didn’t digest what they’d engulfed. Now the researchers are looking for a molecular trigger to get the engineered cells to complete this last task.

Eventually, the scientific team aims to build artificial cells that are programmed to target and destroy abnormal cells, such as those ravaged by bacteria, cancer or other diseases.

Learn more:
Johns Hopkins News Release Exit icon
How Cells Take Out the Trash Article from Inside Life Science
Cellular Suicide: An Essential Part of Life Article from Inside Life Science

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Meet Janet Iwasa

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Janet Iwasa
Credit: Janet Iwasa
Janet Iwasa
Fields: Cell biology and molecular animation
Works at: University of Utah
Raised in: Indiana and Maryland
Studied at: University of California, San Francisco, and Harvard Medical School
When not in the lab she’s: Keeping up with her two preschool-aged sons
Something she’s proud of that she’ll never try again: Baking a multi-tiered wedding cake, complete with sugar flowers, for a friend’s wedding.

Janet Iwasa wouldn’t have described herself as an artistic child. She didn’t carry around a sketch pad, pencils or paintbrushes. But she remembers accompanying her father, a scientist at the National Institutes of Health, to his lab on the weekends. She’d spend hours doodling in a drawing program on his old Macintosh computer while he worked on experiments.

“I always remember wanting to be a scientist, and that’s probably highly inspired by my dad,” says Iwasa. Her early affinity for art and technology set her on an unusual career path to become a molecular animator. A typical work day now finds her adapting computer programs originally designed to bring characters like Buzz Lightyear to life to help researchers probe complicated, dynamic interactions within cells.

Iwasa’s interest in animation was sparked when she was a graduate student in cell biology, studying a protein called actin, which helps cells to move and change shape. At the time, the only visual representations she had of actin networks were flat, two-dimensional drawings on paper. When she saw an animation of the dynamic movement of a molecule called kinesin, she thought, “Why are we relying on oversimplified, static illustrations [of molecules], when we can be doing something like this video?”

Within a year, she was taking an animation class at a local college. She quickly realized that she would need more intensive instruction to be able to animate complex biological processes. A few summers later, she flew to Hollywood for a 3-month training program in industry-standard animation technology.

The oldest student in that course—and the only woman—Iwasa immediately began thinking about how to adapt a standard animator’s toolkit to illustrate the inner life of cells. A technique used to create the effect of human hair blowing in the wind could also show the movement of an RNA molecule. A chunk of computer code used to make the facets of a soccer ball fall apart and come back together in a different order could be adapted to model virus assembly and disassembly.

Her Findings

Following her training, Iwasa spent 2 years as a National Science Foundation Discovery Corps fellow, producing the Exploring Life’s Origins exhibit with the Boston Museum of Science and the Szostak Lab at Massachusetts General Hospital/Harvard Medical School. As part of the multi-media exhibit, she created animations to illustrate how the simplest living organisms may have evolved on early Earth.

Since then, Iwasa has helped researchers model such complex actions as how cells ingest materials, how proteins are transported across a cell membrane, and how the motor protein dynein helps cells divide.

Screenshot from the video that shows how a protein called clathrin forms a cage-like container that cells use to engulf and ingest materials
Iwasa developed this video to show how a protein called clathrin forms a cage-like container that cells use to engulf and ingest materials.

Iwasa calls her animations “visual hypotheses”: The end results may be beautiful, but the process of animation itself is what encapsulates, clarifies and communicates the science.

“It’s really building the animated model that brings insights,” she says. “When you’re creating an animation, you’re really grappling with a lot of issues that don’t necessarily come up by any other means. In some cases, it might raise more questions, and make people go back and do some more experiments when they realize there might be something missing” in their theory of how a molecular process works.

Now she’s working with an NIH-funded research team at the University of Utah to develop a detailed animation of how HIV enters and exits human immune cells.

Abbreviated CHEETAH, the full name of the group is the Center for the Structural Biology of Cellular Host Elements in Egress, Trafficking, and Assembly of HIV.

“In the HIV life cycle, there are a number of events that aren’t really well understood, and people have different ideas of how things happen,” says Iwasa. She plans to animate the stages of viral infection in ways that reflect different proposals for how the process works, to give researchers a new way to visualize, communicate—and potentially harmonize—their hypotheses.

The full set of Iwasa’s HIV-related animations will be available online as they are completed, at https://scienceofhiv.org, with the first set launching in the fall of 2014.

Learn more:
Janet Iwasa’s TED Talk: How animations can help scientists test a hypothesis
Janet Iwasa’s 3D model of an HIV particle was a winner in the 2014 BioArt contest sponsored by Federation of American Societies for Experimental Biology
NIH Director’s blog post about Iwasa and her HIV video animation

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Cool Image: Outsourcing Cellular Housekeeping

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Mouse optic nerve and retina. Credit: Keunyoung Kim, Thomas Deerinck and Mark Ellisman, National Center for Microscopy and Imaging Research, UC San Diego.
This image shows the mouse optic nerve and retina. Credit: Keunyoung Kim, Thomas Deerinck and Mark Ellisman, National Center for Microscopy and Imaging Research Exit icon, UC San Diego.

In this image, the optic nerve (left) leaves the back of the retina (right). Where the retina meets the optic nerve, visual information begins its journey from the eye to the brain. Taking a closer look, axons (purple), which carry electrical and chemical messages, meet astrocytes (yellow), a type of brain cell. Recent research has found a new and surprising role for these astrocytes.

Biologists have long thought that all cells, including neurons, degrade and reuse pieces of their own mitochondria, the little powerhouses that provide energy to cells. Using cutting-edge imaging technology, researchers led by Mark Ellisman of the University of California, San Diego, and Nicholas Marsh-Armstrong of Johns Hopkins University have caught neurons in the mouse optic nerve in the act of passing some of their worn out mitochondria to neighboring astrocytes, which then did the dirty work of recycling.

The researchers also showed that neurons in other regions of the brain appear to outsource mitochondrial breakdown to astrocytes as well. They suggest that it will be important to confirm that this process occurs in other parts of the brain and to determine how possible defects in the outsourcing may contribute to or underlie neuronal dysfunction or neurodegenerative diseases.

This work also was funded by NIH’s National Eye Institute and National Institute on Drug Abuse.

Learn more:
University of California, San Diego News Release and Blog Posting Exit icon
How Cells Take Out the Trash Article from Inside Life Science

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Cool Video: How a Microtubule Builds and Deconstructs

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A microtubule, part of the cell’s skeleton, builds and deconstructs. Credit: Eva Nogales lab, University of California, Berkeley.

In this animation, tubulin proteins snap into place like Lego blocks to build a microtubule, part of the cell’s skeleton. When construction ends, this long hollow cylinder falls to pieces from its top end. The breakdown is critical for many basic biological processes, including cell division, when rapidly shortening microtubules pull chromosomes into each daughter cell.

Until recently, scientists didn’t know exactly what drove microtubules to fall apart. A research team led by Eva Nogales of the Lawrence Berkeley National Laboratory and the University of California, Berkeley, now has an explanation.

Using high-powered microscopy, the scientists peered into the structure of a microtubule and found how a chemical reaction puts the stacking tubulin proteins under intense strain. The only thing keeping the proteins from springing apart is the pressure from the addition of more tubulin. So when assembly stops, the microtubule deconstructs.

The team also learned that Taxol, a common cancer drug, relieves this tension and allows microtubules to remain intact indefinitely. With microtubules frozen in place, a cancer cell cannot divide and eventually dies.

Because of this research, scientists now better understand both the success behind a common cancer drug and the molecular basis underlying the workings of microtubules.

Learn more:
University of California, Berkeley News Release Exit icon
Nogales Lab

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Cool Image: Researching Regeneration in a Model Organism

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The isolated feeding tube of a flatworm.

The feeding tube, or pharynx, of a planarian worm with cilia shown in red and muscle fibers shown in green. Credit: Carrie Adler/Stowers Institute for Medical Research.

This rainbow-hued image shows the isolated feeding tube, or pharynx, of a tiny freshwater flatworm called a planarian, with the hairlike cilia in red and muscle fibers in green. Scientists use these wondrous worms, which have an almost infinite capacity to regrow all organs, as a simple model system for studying regeneration. A research team led by Alejandro Sánchez Alvarado of the Stowers Institute for Medical Research exploited a method known as selective chemical amputation to remove the pharynx easily and reliably. This allowed the team to conduct a large-scale genetic analysis of how stem cells in a planaria fragment realize what’s missing and then restore it. The researchers initially identified about 350 genes that were activated as a result of amputation. They then suppressed those genes one by one and observed the worms until they pinpointed one gene in particular—a master regulator called FoxA—whose absence completely blocked pharynx regeneration. Scientists believe that researching regeneration in flatworms first is a good way to gain knowledge that could one day be applied to promoting regeneration in mammals.

Learn more:
Stowers Institute News Release
Sánchez Lab