It’s time for your weekly dose of cell and molecular biology. As always, I’ve chosen select posts from blogs that I read – please do contact me with specific posts that you’d like “Cells Weekly” to link to, or topical blog discussions might be missing. And of course, please link to the “Cells Weekly” to share it with others.
- Biosingularity: Molecule linked to autoimmune disease relapses identified, Natural protein stops deadly human brain cancer in mice
- The Daily Transcript: How proteins cross the Nuclear Pore Complex, Ribosome-SRP-signal sequence structures
- Pharyngula: Notch
- Omics! Omics!: Computing cancer, Cousin May’s least favorite bacteria
- Ouroboros: Genomic instability and transcriptional noise
- Gene Expression: Dendritic spines! Good God! What are they good for?
- A Blog Around the Clock: From two cells to many: cell differentiation and embryonic development
- We Are Devo!: Bimodality of calcium dependent axon pathfinding
And some ScienceDaily picks:
Vito Quaranta clicks on a small black dot on his computer screen. The dot — which represents about a thousand cancer cells — begins to “grow,” morphing into a mass with finger-like projections that looks like an invasive tumor.
The Vanderbilt professor of cancer biology envisions a future when computer simulations like this will be used to predict a tumor’s clinical progression and formulate individualized treatment plans. For the last two years, he has headed a major effort to develop the kind of mathematical model for cancer invasion powerful enough for this purpose. The result was published as an entirely theoretical paper in the journal Cell and, if he is right, it represents a “sea change” in how biology is done.
Brain cells derived from human embryonic stem cells improved the condition of rats with Parkinson’s-like symptoms dramatically, but the treatment caused a significant problem — the appearance of brain tumors — that scientists are now working to solve. The study is featured on the cover of the November issue of Nature Medicine.
The work was reported by neurologist Steven Goldman, M.D., Ph.D., professor of Neurology at the University of Rochester Medical Center and chief of its Division of Cell and Gene Therapy, and Neeta Roy, Ph.D., assistant professor of Neurology at Cornell’s Weill Medical College.
A protein called NMNAT protects against nerve cell degeneration in fruit flies and mice, said Baylor College of Medicine researchers in a report in the Public Library of Science Biology that appears online today.
The finding begs the question if a drug might be developed that could stimulate extra protein production and thus neuronal protection — both in injured cells and in those degenerating because of disease, said Dr. Hugo Bellen, the paper’s senior author, director of the BCM Program in Developmental Biology and a Howard Hughes Medical Institute investigator. While more work needs to be done to determine whether that would be desirable, Bellen said the finding is an important one because it identifies NMNAT as essential in the life of the body’s neurons.
Researchers at the Salk Institute for Biological Studies in collaboration with scientists at the University of California, San Diego (UCSD) took a high resolution “action shot” of a protein switch that plays a crucial role in the development of the nervous system. Their findings, published in the Dec. 8 issue of the journal Molecular Cell, provide a template for the design of small molecule inhibitors to control that switch, a protein called Scp1, at will.
“Scp1 is an important brake that regulates the transition from neuronal precursor to mature neuron,” explains senior author Joseph Noel, Ph.D, a Howard Hughes Medical Institute investigator at Salk. “Loosening the brake with an inhibitor would allow us to influence the timing of neuronal differentiation,” he adds.