News from the Cell Biology Meeting in San Francisco
Bushwhacking through the cellular jungle, researchers are always relieved to stumble across a known molecular pathway. Imagine their excitement at finding a major intersection in unmapped territory. Antoine Muchir and Howard Worman at the Columbia University College of Physicians & Surgeons in New York and their colleagues in France, have discovered a cellular "crossroads" that links the function of the MAP kinase pathway, long implicated in heart failure, to A-type nuclear lamins. Mutations in LMNA, the gene encoding all A-type lamins, cause at least two heritable diseases that affect the heart: Dilated Cardiomyopathy with conduction system defects (DC) and Emery-Dreifuss Muscular Dystrophy (EDMD), which affects muscles and tendons in addition to causing life-threatening cardiomyopathy and cardiac conduction system defects. Muchir presented the findings Sunday at the 45th Annual Meeting of the American Society for Cell Biology in San Francisco.
Instead of using a machete, these cellular trailblazers followed a mouse. The researchers created a "knock-in" model mouse by replacing the normal mouse LMNA gene with a mutated human gene that causes EDMD. Lamin proteins form a network of filaments inside the nucleus, conferring shape and mechanical stability, but they are also "used" by many other proteins and pathways in the nucleus, for a variety of purposes. Mutations in LMNA cause a wide range of human diseases--besides DC and EDMD, these "laminopathies" include other heritable forms of muscular dystrophy, lipodystrophy, neuropathy, bone disorders and accelerated aging (progeria) syndromes.
John Fleischman | EurekAlert!
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