Overactive Signaling Leads to Abnormal Synapses in Fragile X Syndrome (2 of 2) (IMAGE)

American Association for the Advancement of Science (AAAS)

Overactive Signaling Leads to Abnormal Synapses in Fragile X Syndrome (2 of 2)

Caption

Loss of FMR1 leads to increased BMPR2 abundance. (A) In wild-type neurons, FMRP represses BMPR2, which limits LIMK1 activation and promotes actin depolymerization. (B) In FMRP mutant neurons, BMPR2 levels increase, which drives LIMK1 activation and reduces actin polymerization. This material relates to a paper that appeared in the June 7, 2016, issue of Science Signaling, published by AAAS. The paper, by R. Kashima at University of California, San Francisco in San Francisco, Calif., and colleagues was titled, "Augmented noncanonical BMP type II receptor signaling mediates the synaptic abnormality of fragile X syndrome."

Credit

H. Broihier <i>et al., Science Signaling</i> (2016)

Usage Restrictions

Please cite the owner of the material when publishing. This material may be freely used by reporters as part of news coverage, with proper attribution. Non-reporters must contact <i>Science</i> for permission.

License

Licensed content

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.