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DTSTART:20210328T030000
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DTSTART:20201025T020000
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BEGIN:VEVENT
DTSTAMP:20260405T161908Z
UID:1604406600@ist.ac.at
DTSTART:20201103T133000
DTEND:20201103T140000
DESCRIPTION:Speaker: Thanh VUONG-BRENDER\nhosted by Lora Sweeney\nAbstract:
  " Calmodulin (CaM) is the major calcium ion (Ca2+) sensor in many biologi
 cal processes\, regulating for example the CaM kinases\, calcineurin\, and
  many ion channels. CaM levels are limiting in cells compared to its myria
 d targets\, but how CaM levels are controlled is poorly understood. We fin
 d that CaM abundance in the C. elegans and Drosophila nervous systems is c
 ontrolled by the CaM-binding transcription activator\, CAMTA. C. elegans C
 AMTA (CAMT-1)\, like its fly and mammalian orthologues\, is expressed wide
 ly in the nervous system. camt-1 mutants display pleiotropic behavioural d
 efects and altered Ca2+ signaling in neurons. Using FACS-RNA Seq we profil
 e multiple neural types in camt-1 mutants and find all exhibit reduced CaM
  mRNA compared to controls. Supplementing CaM levels using a transgene res
 cues camt-1 mutant phenotypes. Chromatin immunoprecipitation sequencing (C
 hIP-Seq) data show that CAMT-1 binds several sites in the calmodulin promo
 ter. CRISPR-mediated deletion of these sites shows they redundantly regula
 te calmodulin expression. We also find that CaM can feed back to inhibit i
 ts own expression by a mechanism that depends on CaM binding sites on CAMT
 -1. This work uncovers a mechanism that can both activate and inhibit CaM 
 expression in the nervous system\, and controls Ca2+ signalling\, neuronal
  excitability and behavior."
LOCATION:online\, ISTA
ORGANIZER:sandra.landauer@ist.ac.at
SUMMARY:Thanh VUONG-BRENDER: Transcriptional Control Of Calmodulin By CAMTA
  Regulates Neural Excitability
URL:https://talks-calendar.ista.ac.at/events/2946
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