Opening a new front in the battle against Alzheimer’s disease, scientists at the University of Pennsylvania have found that a protein long associated with the disease inflicts grave damage in a previously unimagined way: It seals off mitochondria in affected neurons, resulting in an “energy crisis” and buildup of toxins that causes cells to die. This pathway, the first specific biochemical explanation for pathologies associated with Alzheimer’s, is detailed in the April 14 issue of the Journal of Cell Biology.
Researchers have produced the first laboratory evidence to show that a cell’s possession of an abnormal numbers of chromosomes contributes to the development of cancers. Their report on the role of this chromosomal instability, known as aneuploidy, appears in today’s online edition of the Feb. 3 Journal of Cell Biology. Because 85 percent of human cancer cells possess an abnormal number of chromosomes, researchers have long been curious about the role of aneuploidy in the multistep cancer process.
Cancer cells move around the body (become metastatic) by chopping up the dense matrix that surrounds them. But drugs that prevent the chopping have been disappointing in animal and human anti-cancer trials. Now researchers provide an explanation for this failure: the drug-treated cells revert to a primordial, ameboid form of cell movement that allows them to squeeze through gaps in the matrix.
This is a little complex, but bear with us. Nearly all cells house their DNA inside a nucleus. But a little one-celled critter called Tetrahymena houses different versions of its DNA in each of its two nuclei. Researchers have found that the smaller nucleus (called the micronucleus) just keeps the cell’s full genome safe, acting as a sort of “lock box.” The larger nucleus (called the macronucleus) uses the DNA to regulate the cell’s life functions. When the cell mates to create a new generation, the two work together to compare the cell’s current DNA against what’s been stored in the lock box. If any foreign genes have snuck in (like from a virus) they nuclei eliminate it, to make sure baby gets a fresh start. Pretty neat, with possible implications for larger organisms, too.
Pre-cells destined to become fat can be converted instead into true bone cells in
response to outside signals, say researchers at the University of California, San Francisco. The finding could pave the way for scientists to replenish lost bone cells in patients with conditions like osteoporosis, and to help repair bone defects. The new bone cells have all the hallmarks associated with mature bone formation, including production of bone proteins and calcification, the UCSF team says.