Getting the embryo into shape
نویسنده
چکیده
Membrane backtracking T he inner membrane of a chloroplast bristles with enzymes and other proteins that are synthesized in the cytoplasm, but how they get into position is uncertain. On page 249, Li and Schnell report that at least some proteins pass through the inner membrane and reenter it from the back side, rather than stopping on the way through. Chloroplasts are swaddled by inner and outer membranes and contain a third membrane system, the thylakoid, where photosynthesis occurs. Most of the proteins in these membranes are made in the cytoplasm. Proteins can slip directly into the outer membrane. But the journey to the inner membrane is more complicated because proteins must traverse the outer membrane and avoid piercing the thylakoid layer. Li and Schnell followed the path of atTic40, which is part of an inner membrane protein complex that helps usher others through the barrier. They found that chloroplasts import an elongated version of atTic40 that accumulates fully inside the chloroplast before moving back into the inner membrane. The scientists also demonstrated that atTic40 can integrate into isolated inner membranes, indicating that import of the proteins and their insertion into the inner membrane are independent. Chloroplasts have thus evolved a sorting system that can distinguish inner membrane and thylakoid proteins. Getting the embryo into shape S ome stem cells in the embryo have the same effect as a personal trainer, show Gerhart et al. on page 283. Although they are candidates for forming muscle cells themselves, they instead coax others to build the muscle. Muscle-promoting cells might thus emerge earlier in development than many researchers thought. When a chick embryo is only a two-layered disk, the upper layer called the epiblast already houses a few cells that have turned on the gene for MyoD, one of the supervisors for muscle development. But the cells also manufacture another muscle stimulator, known as Noggin. In the culture dish, these cells prod unprogrammed cells to form muscle. To investigate the cells' function in bulking up the embryo, Gerhart et al. tracked them with antibodies. Most of the MyoD producers ended up in the somites that give rise to muscle throughout the body. The researchers then destroyed the MyoD cells in the epiblast and followed the developmental consequences. The loss reduced the amount of skeletal muscle, weakening the trunk muscles so much that organs bulged through the body wall. Implanting beads saturated with …
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عنوان ژورنال:
- The Journal of Cell Biology
دوره 175 شماره
صفحات -
تاریخ انتشار 2006