Snapshots of Life: Wild Outcome from Knocking Out Mobility Proteins

Spiky fibroblast cell

Credit: Praveen Suraneni and Rong Li, Stowers Institute for Medical Research

When biologists disabled proteins critical for cell movement, the result was dramatic. The membrane, normally a smooth surface enveloping the cell, erupted in spiky projections. This image, which is part of the Life: Magnified exhibit, resembles a supernova. Although it looks like it exploded, the cell pictured is still alive.

To create the image, Rong Li and Praveen Suraneni, NIH-funded cell biologists at the Stowers Institute for Medical Research in Kansas City, Missouri, disrupted two proteins essential to movement in fibroblasts—connective tissue cells that are also important for healing wounds. The first, called ARPC3, is a protein in the Arp2/3 complex. Without it, the cell moves more slowly and randomly [1]. Inhibiting the second protein gave this cell its spiky appearance. Called myosin IIA (green in the image), it’s like the cell’s muscle, and it’s critical for movement. The blue color is DNA; the red represents a protein called F-actin.

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Happy Birthday, Jane Goodall!

Jane Goodall with Freud

Credit: Michael Neugebauer, courtesy of The Jane Goodall Institute
Caption: Dr. Jane Goodall with Freud, a Gombe chimpanzee

Today, I’d like to wish a very “Happy Birthday” to a dear friend and one of my personal heroes: Jane Goodall. Given Jane’s energy and youthful attitude, it’s hard to believe that this scientist who was so instrumental in advancing our understanding of primate behavior is turning 80 today.

But, indeed, more than a half-century has passed since Jane first traveled to Africa to begin her field research in Gombe National Park on the shores of Africa’s Lake Tanganyika. Her goal? To observe wild chimpanzees in their natural environment and analyze their behavior like no researcher had done before.

At first, the chimps were shy and ran away whenever Jane approached. But, as they grew used to the young biologist’s presence, they continued on with their daily activities as she carefully watched and meticulously recorded their actions, often equipped with nothing more than a pair of binoculars, a pencil, and a notebook. Her landmark work revealed that chimp behavior resembled human behavior in ways that no one had even imagined—findings that transformed our understanding of our closest relatives in the animal kingdom. Continue reading

Creative Minds: Interpreting Your Genome

Artist's rendering of a doctor with a patient and a strand of DNA

Credit: Jane Ades, National Human Genome Research Institute, NIH

Just this year, we’ve reached the point where we can sequence an entire human genome for less than $1,000. That’s great news—and rather astounding, since the first human genome sequence (finished in 2003) cost an estimated $400,000,000!  Does that mean we’ll be able to use each person’s unique genetic blueprint to guide his or her health care from cradle to grave?  Maybe eventually, but it’s not quite as simple as it sounds.

Before we can use your genome to develop more personalized strategies for detecting, treating, and preventing disease, we need to be able to interpret the many variations that make your genome distinct from everybody else’s. While most of these variations are neither bad nor good, some raise the risk of particular diseases, and others serve to lower the risk. How do we figure out which is which?

Jay Shendure, an associate professor at the University of Washington in Seattle, has an audacious plan to figure this out, which is why he is among the 2013 recipients of the NIH Director’s Pioneer Award.

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siRNAs: Small Molecules that Pack a Big Punch

Photo of parkin protein (green) that tags damaged mitochondria (red)

Caption: NIH scientists used RNA interference to find genes that interact with the parkin protein (green), which tags damaged mitochondria (red). Mutations in the parkin gene are linked to Parkinson’s disease and other mitochondrial disorders.
Credit: Richard J. Youle Laboratory, NINDS, NIH

It would be terrific if we could turn off human genes in the laboratory, one at a time, to figure out their exact functions and learn more about how our health is affected when those functions are disrupted. Today, I’m excited to announce the availability of new data that will empower researchers to do just that on a genome-wide scale. As part of a public-private collaboration between the NIH’s National Center for Advancing Translational Sciences (NCATS) and Life Technologies Corporation, researchers now have access to a wealth of information about small interfering RNAs (siRNAs), which are snippets of ribonucleic acid (RNA) with the power to turn off a gene, or reduce its activity—in much the same way that we use a dimmer switch to modulate a light.

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Copying and Reading the Book of Life Inside One Cell, Accurately

Microwell strip

Caption: The genome researchers collaborated with materials science engineers to create the arrays of microwells or compartments that each capture a single cell.
Credit: UC San Diego Jacobs School of Engineering

Decoding the complete DNA genome in a single cell has been a major goal of technology developers. But the methods aren’t quite able to deal with that yet.  So, for scientists to do this, they first need to make multiple copies of the DNA inside. Until now, the copying technology hasn’t been as accurate as scientists would like. If you think of the genome like a book, then our current copiers replicate certain chapters thousands of times, others just a few, and some not at all. As you can imagine, if you tried to read one of these copies, you’d be quite confused—and you certainly couldn’t rely on your reading for any medical purposes.

Now, NIH-funded researchers at the University of California, San Diego, have developed a new molecular technique that can accurately and uniformly copy the DNA inside a single cell [1]. Using this technique, they’ve already made some surprising discoveries.

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