Scientists have long held theories about the importance of proteins called B-type lamins in the process of embryonic stem cells replicating and differentiating into different varieties of cells. New research from a multi-institutional team led by the Carnegie Institution for Science’s Dr. Yixian Zheng indicates that, counter to expectations, these B-type lamins are not necessary for stem cells to renew and develop, but are necessary for proper organ development. The team’s work was published on November 24, 2011 in Science Express. Nuclear lamina is the material that lines the inside of a cell's nucleus. Its major structural component is a family of proteins called lamins, of which B-type lamins are prominent members and thought to be absolutely essential for a cell's survival. Mutations in lamins have been linked to a number of human diseases. Lamins are thought to suppress the expression of certain genes by binding directly to the DNA within the cell's nucleus. The role of B-type lamins in the differentiation of embryonic stem cells into various types of cells, depending on where in a body they are located, was thought to be crucial. The lamins were thought to use their DNA-binding suppression abilities to tell a cell which type of development pathway to follow. But the research team--including Carnegie's Drs. Youngjo Kim, Katie McDole, and Chen-Ming Fan--took a hard look at the functions of B-type lamins in embryonic stem cells and in live mice. They found that, counter to expectations, B-type lamins were not essential for embryonic stem cells to survive, nor did their DNA binding directly regulate the genes to which they were attached. However, mice deficient in B-type lamins were born with improperly developed organs—including defects in the lungs, diaphragms, and brains—and were unable to breathe.
Huntington's disease (HD) is characterized by ongoing destruction of specific neurons within the brain. It affects a person's ability to walk, talk, and think - leading to involuntary movement and loss of muscle coordination. New research, published on November 25, 2011 in BioMed Central's open access journal Molecular Neurodegeneration, shows that the RyanR inhibitor Dantrolene is able to reduce the severity of walking and balance problems in a mouse model of HD. Progressive damage to medium spiny neurons (MSN) in the brain of a person with HD is responsible for many of the symptoms and is caused by an inherited recessive mutation in the gene 'Huntingtin.’ The mutated version of this protein leads to abnormal release of calcium from stores within the neurons which in turn disrupts the connections between neurons firing and muscle contractions, and eventually kills the neurons. Researchers from the University of Texas Southwestern Medical Center, and colleagues, tested Dantrolene, a muscle relaxant which works by stabilizing calcium signaling, and showed that this drug could prevent calcium-dependent toxicity in laboratory-grown neurons. The team led by Dr. Ilya Bezprozvanny also found that Dantrolene could prevent destruction of coordination, measured by beam walking and footprint patterns, in mice with Huntington's-like disease. Dr. Bezprozvanny explained, "One of the features of HD mice is the progressive loss of their NeuN-positive neurons. Dantrolene was not only able to protect muscle coordination in mice with HD, but also prevented destruction of NeuN-positive neurons.
Each fall millions of monarch butterflies from across the eastern United States use a time-compensated sun compass to direct their navigation south, traveling up to 2,000 miles to an overwintering site in a specific grove of fir trees in central Mexico. Scientists have long been fascinated by the biological mechanisms that allow successive generations of these delicate creatures to traverse such long distances to a small region roughly 300 square miles in size. To unlock the genetic and regulatory elements important for this remarkable journey, neurobiologists at the University of Massachusetts Medical School (UMMS) are the first to sequence and analyze the monarch butterfly genome. "Migratory monarchs are at least two generations removed from those that made the journey the previous fall," said Dr. Steven M. Reppert, professor and chair of neurobiology and senior author of the study. "They have never been to the overwintering sites before, and have no relatives to follow on their way. There must be a genetic program underlying the butterflies' migratory behavior. We want to know what that program is, and how it works." In a paper featured as the cover article of the November 23, 2011 issue of Cell, Dr. Reppert and UMMS colleagues Dr. Shuai Zhan, and Dr. Christine Merlin, along with collaborator Dr. Jeffrey L. Boore, CEO of Genome Project Solutions in Hercules, California, describe how next-generation sequencing technology was used to generate a draft 273 Mb genome of the migratory monarch. Analysis of the combined genetic assembly revealed an estimated set of 16,866 protein-coding genes, comprising several gene families likely involved in major aspects of the monarch's seasonal migration. The novel insights gained by Dr.