Synaptic BMAL1 phosphorylation controls circadian hippocampal plasticity-Reference-Cited by-同舟云学术

Synaptic BMAL1 phosphorylation controls circadian hippocampal plasticity

Published:2023-10-27 Issue:43 Volume:9 Page:
ISSN:2375-2548
Container-title:Science Advances
language:en
Short-container-title:Sci. Adv.

Author:

Barone Ilaria¹^ORCID,Gilette Nicole M.¹^ORCID,Hawks-Mayer Hannah¹,Handy Jonathan¹^ORCID,Zhang Kevin J.¹^ORCID,Chifamba Fortunate F.¹^ORCID,Mostafa Engie¹^ORCID,Johnson-Venkatesh Erin M.¹^ORCID,Sun Yan¹,Gibson Jennifer M.²,Rotenberg Alexander¹,Umemori Hisashi¹^ORCID,Tsai Peter T.²^ORCID,Lipton Jonathan O.¹³^ORCID

Affiliation:

1. Department of Neurology and F.M. Kirby Center for Neurobiology, Boston Children’s Hospital, Boston, MA 02115, USA.

2. Departments of Neurology, Neuroscience, Pediatrics, and Psychiatry, University of Texas at Southwestern, Dallas, TX 75390, USA.

3. Department of Neurology and Division of Sleep Medicine, Harvard Medical School, Boston, MA 02115, USA.

Abstract

The time of day strongly influences adaptive behaviors like long-term memory, but the correlating synaptic and molecular mechanisms remain unclear. The circadian clock comprises a canonical transcription-translation feedback loop (TTFL) strictly dependent on the BMAL1 transcription factor. We report that BMAL1 rhythmically localizes to hippocampal synapses in a manner dependent on its phosphorylation at Ser 42 [pBMAL1(S42)]. pBMAL1(S42) regulates the autophosphorylation of synaptic CaMKIIα and circadian rhythms of CaMKIIα-dependent molecular interactions and LTP but not global rest/activity behavior. Therefore, our results suggest a model in which repurposing of the clock protein BMAL1 to synapses locally gates the circadian timing of plasticity.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Link

https://www.science.org/doi/pdf/10.1126/sciadv.adj1010

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