Neutrophils are the most abundant type of white blood cell. They play a vital role in defending us from infections, by engulfing and destroying bacteria and viruses or cancerous cells. A new study by UC Davis engineering student Emmet Francis, working with Professor Volkmar Heinrich in the Department of Biomedical Engineering, adds to our knowledge of how neutrophils are drawn towards infection sites and how they can attack their targets.
First, Francis and Heinrich looked at how isolated neutrophils respond to chemical messengers called anaphylatoxins. These molecules guide immune cells to their targets but can cause severe illness in excessive amounts.
By Greg Watry
Within every cell is a transportation system that rivals our most complex roadways and interchanges. Known collectively as the cytoskeleton, this system is used by molecular machines called motor proteins to transport cargo throughout the cell. It’s also essential to the vital process of cell division.
Image of the mitotic spindle in a human cell showing microtubules in green, chromosomes (DNA) in blue, and kinetochores in red. (Wikimedia Commons)
By Holly Ober
A new technique developed at UC Davis may have broken the barrier to rapid assembly of pure protein synthesis machinery outside of living cells.
E. coli bacteria tagged with different colors produced different mixtures of proteins. Together, the bacterial consortium makes all the proteins needed for mRNA translation/protein synthesis (Fernando Villarreal, UC Davis)
In order to reconstitute cellular reactions outside of biological systems, scientists need to produce the proteins involved. Rapid yet high purity reconstitution of the cellular reactions is critical for the high-throughput study of cellular pathways and cell-free diagnostic tests for various diseases. Reconstituting cellular reactions outside cells, however, requires the separate expression and purification of each protein required to execute the reactions. This process is expensive and time consuming, making the production of more than several proteins at once extremely challenging.
By David Slipher
Assistant Professor Sean Collins, Department of Microbiology and Molecular Genetics in the UC Davis College of Biological Sciences, has received a $1.5 million award from the National Institutes of Health to advance the development of “smart” immune cells for therapies to treat cancer and other diseases. The five-year NIH Director’s New Innovator Award aims to provide new insight into how to engineer immune cells to control their recruitment and response to tumors.
Assistant professor Sean Collins has received a NIH New Innovator award for work to make cancer therapies safer. Fred Greaves, UC Davis
Homologous Recombination Can Cause More Breaks As It Fixes Them
The traditional view of cancer is that a cell has to sustain a series of hits to its DNA before its defenses break down enough for it to turn cancerous. But cancer researchers have also found that cells can experience very rapid and widespread DNA damage that could quickly lead to cancer or developmental defects.
Now researchers at the University of California, Davis, have found that these complex chromosomal rearrangements can be triggered in a single event when a process used to repair DNA breaks, homologous recombination, goes wrong. The work is published Aug. 10 in the journal Cell.
By Kathy Keatley Garvey
Researchers in Professor Bruce Hammock’s laboratory at UC Davis are studying mechanisms involved in blocking angiogenesis — the formation of new blood vessels. The findings may lead to new methods for preventing cancer growth and targeting other diseases, the researchers report.
Postdoc Amy Rand is studying how certain fats can affect growth of blood vessels in tumors.
A recently-published study from Hammock’s lab describes a novel lipid-signaling molecule that can change fundamental biological processes involved in human health and disease. It builds on landmark research by the Judah Folkman laboratory of Harvard Medical School, which earlier showed that cutting off blood vessels that feed a cancerous tumor could stop its growth.
Where would we be without meiosis and recombination? For a start, none of us sexually reproducing organisms would be here, because that’s how sperm and eggs are made. And when meiosis doesn’t work properly, it can lead to infertility, miscarriage, birth defects and developmental disorders.
Neil Hunter’s laboratory at the UC Davis College of Biological Sciences is teasing out the complex details of how meiosis works. In a new paper published online Jan. 6 in the journal Science, Hunter’s group describes new key players in meiosis, proteins called SUMO and ubiquitin and molecular machines called proteasomes. Ubiquitin is already well-known as a small protein that “tags” other proteins to be destroyed by proteasomes (wood chippers for proteins). SUMO is a close relative of ubiquitin.
Full post: New Steps in the Meiosis Chromosome Dance
(809 words, 2 images, estimated 3:14 mins reading time)
“Gnothi seauton” or “Know thyself,” said the Ancient Greeks; but they might have also said, “eat yourself.” For biologists, autophagy or “self-eating” is the process that cells use to recycle material inside the cell. It breaks down defective proteins and molecules, disposes of invading viruses and bacteria, provides an energy source when food is lacking and generally keeps cells fit and healthy. Problems in autophagy are implicated in cancer, aging, infectious disease and degenerative disorders.
Yoshinori Ohsumi after hearing he had been awarded the 2016 Nobel Prize in Physiology or Medicine.
Photo: Mari Honda
Full post: Nobel Medicine Prize for “self-eating”
(307 words, 1 image, estimated 1:14 mins reading time)
UC Davis researchers have developed a way to use the empty shell of a Hepatitis E virus to carry vaccines or drugs into the body. The technique has been tested in rodents as a way to target breast cancer, and is available for commercial licensing through UC Davis Office of Research.
Hepatitis E virus is feco-orally transmitted, so it can survive passing through the digestive system, said Marie Stark, a graduate student working with Professor Holland Cheng in the UC Davis Department of Molecular and Cell Biology.
Some of the world’s leading experts in how DNA is protected and repaired from damage will meet at UC Davis Feb. 12-13 for a symposium in honor of Stephen Kowalczykowski, distinguished professor of microbiology and molecular genetics at the UC Davis College of Biological Sciences. Registration information is available here.
“Genome maintenance” is essential to life, said Frederic Chedin, Professor of Molecular and Cellular Biology, who is co-organizer of the symposium with Professors Wolf-Dietrich Heyer and Neil Hunter, Department of Microbiology and Molecular Genetics. Every second of the day, our DNA sustains damage for example from chemicals, radiation or just natural processes inside the cell. Breaks and lesions in DNA can lead to cancer, disease and developmental defects. Living things, from bacteria to plants to people, have evolved a fundamentally similar set of tools and processes that constantly defend and repair DNA.