Posts tagged cell division
Articles and news from the latest research reports.
Impaired cell division leads to neuronal disorder
Prof. Erich Nigg and his research group at the Biozentrum of the University of Basel have discovered an amino acid signal essential for error-free cell division. This signal regulates the number of centrosomes in the cell, and its absence results in the development of pathologically altered cells. Remarkably, such altered cells are found in people with a neurodevelopmental disorder, called autosomal recessive primary microcephaly. The results of these investigations have been published in the current issue of the US journal “Current Biology”.
Cell division is the basis of all life. Of central importance is the error-free segregation of genetic material, the chromosomes. A flawless division process is a prerequisite for the development of healthy, new cells, whilst errors in cell division can cause illnesses such as cancer. The centrosome, a tiny cell organelle, plays a decisive role in this process.
Prof. Erich Nigg’s research group at the Biozentrum of the University of Basel has investigated an important step in cell division: the duplication of the centrosome and its role in the correct segregation of the chromosomes into two daughter cells. The protein STIL has an essential function in this process. It ensures that centrosome duplicate before one half of the genetic material is transported into each of the two daughter cells.
KEN-Box important for protein breakdown
During cell division, the protein STIL is degraded. If this does not occur, the protein accumulates in the cell, which then causes an overproduction of centrosomes. As a consequence, mis-segregated chromosomes are incorporated into the daughter cells, which then represent cells with faulty genetic material. The scientists discovered an amino acid signal on the STIL protein, a so-called KEN-Box, and showed that this is critical for the breakdown of the protein: “The Ken-Box is the signal that orders the protein degradation machinery to break down the STIL protein,” explains Christian Arquint, the first author of this publication. In the absence of the KEN-Box, the protein is not degraded.
Absence of the KEN-Box causes microcephaly
In some patients with microcephaly, a neuronal disorder that leads to a reduced number of nerve cells being produced and, therefore, a smaller brain, the KEN-box is lacking from the STIL protein. The scientists were thus able to demonstrate a tantalizing connection between the absence of this particular amino acid signal and an illness. “When during our investigations of cell division and centrosome duplication we came across a connection to the disorder microcephaly, we were particularly pleased, as this helps us to better understand how this disorder develops“, says Christian Arquint.
In the future, the research group led by Erich Nigg plans to uncover other connections between errors of cell division and the illness microcephaly. They also want to focus on the investigation of other proteins that play important roles in the process of cell division, in particular those involved in centrosome duplication.
Cell biologists show molecular forces are key to proper cell division
Studies led by assistant professor of Biology Thomas Maresca are revealing new details about a molecular surveillance system that helps detect and correct errors in cell division that can lead to cell death or human diseases. Findings are reported in the current issue of the Journal of Cell Biology.
The purpose of cell division is to evenly distribute the genome between two daughter cells. To achieve this, every chromosome must properly interact with a football-shaped structure called the spindle. However, interaction errors between the chromosomes and spindle during division are amazingly common, occurring in 86 to 90 percent of chromosomes, says Maresca, an expert in mitosis.
“This is not quite so surprising when you realize that every single one of the 46 chromosomes has to get into perfect position every time a cell divides,” he notes. The key to flawless cell division is to correct dangerous interactions before the cell splits in two.
Working with fruit fly tissue culture cells, Maresca and graduate students Stuart Cane and Anna Ye have developed a way to watch and record images of the key players in cell division including microtubule filaments that form the mitotic spindle and sites called kinetochores that mediate chromosome-microtubule interactions. They also examined the contribution of a force generated by molecular engines called the polar ejection force (PEF), which is thought to help line up the chromosomes in the middle of the spindle for division. For the first time, they directly tested and quantified how PEF, in particular, influences tension at kinetochores and affects error correction in mitosis.
“We also now have a powerful new assay to get at how this tension regulates kinetochore-microtubule interactions,” Maresca adds. “We knew forces and tension regulated this process, but we didn’t understand exactly how. With the new technique, we can start to dissect out how tension modulates error correction to repair the many erroneous attachment intermediates that form during division.”
New form of cell division found
Researchers at the University of Wisconsin Carbone Cancer Center have discovered a new form of cell division in human cells.
They believe it serves as a natural back-up mechanism during faulty cell division, preventing some cells from going down a path that can lead to cancer.
"If we could promote this new form of cell division, which we call klerokinesis, we may be able to prevent some cancers from developing," says lead researcher Dr. Mark Burkard, an assistant professor of hematology-oncology in the department of medicine at the UW School of Medicine and Public Health.
Burkard presented the finding on Monday, Dec. 17 at the annual meeting of the American Society for Cell Biology in San Francisco.
(View a short video of the process here)
Separation of a cell
This illustration shows a cell undergoing mitosis or “cell division.” The cell membrane is shown in blue, and the cell’s chromosomes are shown in yellow. Mitosis is a well-studied and well-imaged phenomenon in two-dimensional images, but it’s never before been seen quite like this. What makes this image special is the use of a new fluorescent protein called MiniSOG, shown flying out of the cell.
Image courtesy of Andrew Noske and Thomas Deerinck (National Center for Microscopy and Imaging Research, University of California, San Diego); Horng Ou and Clodagh O’Shea (Salk Institute).
(Source: MSNBC)
The adult human circulatory system contains between 20 and 30 trillion red blood cells (RBCs), the precise size and number of which can vary from person to person. Some people may have fewer, but larger RBCs, while others may have a larger number of smaller RBCs. Although these differences in size and number may seem inconsequential, they raise an important question: Just what controls these characteristics of RBCs?
By analyzing the results of genome-wide association studies (GWAS) in conjunction with experiments on mouse and human red blood cells, researchers in the lab of Whitehead Institute Founding Member Harvey Lodish have identified the protein cyclin D3 as regulating the number of cell divisions RBC progenitors undergo, which ultimately affects the resulting size and quantity of RBCs. Their findings are reported in the September 14 issue of Genes and Development.
The gears that help cells divide are coming into clearer focus. Researchers have used a new type of super-resolution microscopy to zoom in on centrosomes, which anchor the fibers that enable chromosomes to separate during cell division. Centrosomes have intrigued scientists since their discovery in the late 1800s, in part because cancer cells often amass extra copies of the structures. But they’re so tiny that they’re barely visible through traditional light microscopes, and researchers haven’t nailed down how they form and what role they play in cancer. So cell biologist David Glover of the University of Cambridge in the United Kingdom and his postdoc Jingyan Fu turned to three-dimensional structured illumination microscopy to provide sharper portraits of centrosomes and to pinpoint several proteins they harbor. Each centrosome consists of two cylindrical components called centrioles shrouded by a molecular cloud, which balloons when cells start the process of division. As the team reveals online today in Open Biology, many of the cloud proteins first gather on the centrioles, moving into the cloud once division begins. That’s the case with the protein Cnn (green), shown above close to the cylindrical centriole (top) and dispersed in the cloud (bottom, inset). With further research, scientists might be able to determine how different proteins interact to construct centrosomes. “We can put the molecular jigsaw together,” Glover says.
It’s a longstanding question in biology: How do cells know when to progress through the cell cycle? In simple organisms such as yeast, cells divide once they reach a specific size. However, determining if this holds true for mammalian cells has been difficult, in part because there has been no good way to measure mammalian cell growth over time.
A team of MIT and Harvard Medical School (HMS) researchers has precisely measured the growth rates of single cells, allowing them to answer that fundamental question. In the Aug. 5 online edition of Nature Methods, the researchers report that mammalian cells divide not when they reach a critical size, but when their growth rate hits a specific threshold.