A fly lamin gene is both like and unlike human genesJune 13, 2007Mitch Dushay and colleagues at Uppsala University in Sweden announce the publication of their paper, "Characterization of lamin Mutation Phenotypes in Drosophila and Comparison to Human Laminopathies" in the June 13th issue of the online, open-access journal PLoS ONE. Lamins are intermediate filament proteins that make up a matrix underlying the nuclear membrane. Mammals have two types of lamins; A-type lamins are expressed in differentiating cells, while B-type lamins are expressed ubiquitously. Mutations in the gene coding for human lamin A cause a range of diseases collectively called laminopathies, including forms of muscular dystrophy and premature aging diseases. The fruit fly Drosophila melanogaster has 2 lamin genes that are expressed in A- and B-type patterns, and it has been assumed that similarly expressed lamins perform similar functions. Yet, Dushay and his colleagues, among others, have shown that the fly lamin genes are more closely related to each other than to mammalian lamin genes. While the independent evolution of similar expression patterns must have been driven by similar vital lamin gene functions, Dushay et el. found that mutations in the ubiquitously expressed Drosophila lamin gene cause larvae to move less and show subtle muscle defects, while surviving lamin adults walk poorly and can't fly - like aged wild type flies. This suggests that lamin mutations might cause neuromuscular defects, premature aging, or both. The resemblance of Drosophila lamin phenotypes to human laminopathies provides an interesting case of gene expression and function diverging through evolution, and promises greater insight into lamin function, and possibly into laminopathic diseases and aging. Public Library of Science |
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| Related Lamin Current Events and Lamin News Articles Scientists deconstruct cell division The last step of the cell cycle is the brief but spectacularly dynamic and complicated mitosis phase, which leads to the duplication of one mother cell into two daughter cells. In mitosis, the chromosomes condense and the nucleus breaks down. Turning down gene expression promotes nerve cell maintenance Anyone with a sweet tooth knows that too much of a good thing can lead to negative consequences. The same can be said about the signals that help maintain nerve cells, as demonstrated in a new study of myelin, a protein key to efficient neuronal transmission. Lamin B locks up Oct-1 A large fraction of the transcription factor Oct-1 is associated with the inner nuclear envelope, but how and why it is retained there was unknown. Lamin A/C deficiency is 'unnerving' Mutations in the nuclear intermediate filament lamin A/C (LMNA) gene are associated with Emery-Dreifuss muscular dystrophy, but cause the disease by unknown mechanisms. Méjat et al. show that one mechanism involves the disruption of neuromuscular junctions. Bowel cancer indicator should lead to better treatment STEM cell scientists have developed a more accurate way of identifying aggressive forms of bowel cancer, which should eventually lead to better treatment and survival rates. Stem cell indicator for bowel cancer should lead to better survival rates Stem cell scientists have developed a more accurate way of identifying aggressive forms of bowel cancer, which should eventually lead to better treatment and survival rates. Bowel cancer is the third most common cancer in the UK. Study finds HIV protease inhibitor drugs may adversely affect the scaffolding of the cell nucleus UCLA scientists, along with collaborators from Purdue University, have demonstrated that HIV protease inhibitors - crucial drugs for HIV treatment - block a cellular enzyme important for generating the structural scaffolding for the cell nucleus. New clues for treatment of disease that causes accelerated aging There is renewed hope for treatment of a rare genetic condition that causes rapidly accelerated aging and leads to an average life expectancy of 13 years. Genetics of muscular dystophy Various forms of human muscular dystrophy result from mutations in genes encoding proteins of the nuclear envelope. A new paper in the February 15th issue of G&D reveals how. Zeroing in on progeria: How mutant lamins cause premature aging Children diagnosed with Hutchinson-Gilford Progeria Syndrome (HGPS) race through life against an unfairly fast clock. Cases are extremely rare-one in 8 million births-but time plays cruel tricks on HGPS newborns. More Lamin Current Events and Lamin News Articles |
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