Genetics & Molecular Biology
Researchers from the Mayo Clinic and the University of Iowa say that the key to bringing obesity under control is to make our muscle a little less efficient and they may have found a way to do it. In a new study in the January issue of Cell Metabolism, the team discusses the possibility that treatments designed to disrupt so-called sarcolemmal ATP-sensitive K+ (KATP) channels specifically in muscles might allow us to control our weight by increasing the number of calories our muscles will burn with regular activity or exercise.
Getting back on my feet after the holiday rush and the expansion of our family: A meeting was held in mid-December
to examine "The Impact of Modeling on Biomedical Research." This was held under the umbrella of the IMAG
and the MSM
The acronyms stand for Interagency Modeling and Analysis Group and the MultiScale Modeling Consortium, which are being operated by various federal science agencies, with the goal of helping the biomedical sciences get serious about modeling.
The autotrophic cell is the one who is able to produce, by it self, its own energy and structural components. It corresponds, in the natural world to the vegetable cell. We call to this process photosynthesis and the wonderful -and truly amazing feature- of this natural phenomena, is that while the income needed for it is inorganic, the final product corresponds to the organic biochemistry world.
(based on So, S., et al. "Autophosphorylation at serine 1981 stabilizes ATM at DNA damage sites." Journal of Cell Biology, early release - published December 21, 2009, 10.1083/jcb.200906064)
(Hopefully 1st in a series of molecular biology topics, explained)
“You gotta know when to hold ‘em. Know when to fold ‘em.” It’s an old adage that every experienced poker player knows. The main goal is to play the game successfully and maximize your profits.
But what if that game is life, and cruel, impersonal genetics is the dealer? There is no luxury of folding your hand and waiting for the next one. People with genetic diseases need to find a way to play the hand that they’re dealt. Fortunately, new scientific research is helping explain the rules of the game, especially for the genetic disease called Huntington’s Disease (HD).
One of the most common hypotheses that I hear with regard to possible non-coding DNA function is that it serves to protect genes against mutation. Junk DNA, according to this proposal, is there to provide a defensive shield against mutagens (usually this includes UV, ionizing radiation, chemical mutagens, viruses, and/or oxygen radicals). I am very skeptical of this explanation, but I am willing to take it seriously if it is studied seriously. In fact, one of my current graduate students first came to talk with me when he was an undergraduate and asked me about this possible function.
Today's issue of Molecular Cell
has two complementary papers on biological signal processing that look interesting (subscription required):
"The Incoherent Feedforward Loop Can Provide Fold-Change Detection in Gene Regulation"
Molecular biologists and mathematical models frequently don't mix well, especially when the molecular biologists in question were trained before the rise of genomics, back when most labs only needed a computer for designing new vector sequences, writing papers, and checking email. Behind this skepticism is the intuition that biology is extremely messy (true), and difficult to quantify (also true). Also contributing is the long history of the cell as a molecular black box; for a long time, we had no idea what was going on inside the cell in molecular terms (somewhat analogous to doing chemistry without knowing about atoms), and in fact we still don't know the molecular role of a good chunk of the protein-coding genes in the human genome.
Dear Mickey - How is life? Life is tough, says my friend. Do you agree? I wanted to write to you for a number of reasons. Believe it or not, people still remember that you turned 80 last year: Happy Eighties to you, M-I-C-K-E-Y!