Prostaglandins (PGs) are lipid signaling molecules that regulate a wide range of processes, such as inflammation, pain, and hormone regulation. One target of PGs is the actin cytoskeleton, but how PGs affect actin filament polymerization and dynamics is not well understood. A recent paper uses the fruit fly egg chamber as a great model of how PGs regulate actin. In the fruit fly egg chamber, many nurse cells surround the oocyte (developing egg). These nurse cells are squeezed in order to dump all of their cytoplasmic contents through ring canals and into the growing egg. During this process, the nuclei of nurse cells are held in place by bundles of actin filaments to ensure that the nuclei don’t plug up the ring canals and block the transfer of the cytoplasm. PGs are an important part of this process, and they interact with an actin-bundling protein called Fascin, according to a recent paper by Groen and colleagues. Inhibition of either Fascin or Pxt, an enzyme required for PG production, results in the failure of actin bundle formation and nurse cell dumping. The loss of Fascin enhances the effects of Pxt reduction, and the overexpression of fascin suppresses the defects seen in flies with Pxt loss. Groen and colleagues show that PGs regulate Fascin, which modulates actin cytoskeleton rearrangements during nurse cell dumping. In the images above, control egg chambers (top) show parallel actin bundles (white) within nurse cells, which extend from the cell membranes to the nuclei (blue). pxt and fascin mutants (middle, bottom), however, contain little to no actin bundles in nurse cells.

Gorgeous one today! I still can't read prostaglandins without hearing the Oklahoma parody in my head.
ReplyDeleteI know, isn't it puuuuurty?!
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