Abstract：
:During muscle regeneration, the mechanism integrating environmental cues at the chromatin of muscle progenitors is unknown. We show that inflammation-activated MKK6-p38 and insulin growth factor 1 (IGF1)-induced PI3K/AKT pathways converge on the chromatin of muscle genes to target distinct components of the muscle transcriptosome. p38 alpha/beta kinases recruit the SWI/SNF chromatin-remodeling complex; AKT1 and 2 promote the association of MyoD with p300 and PCAF acetyltransferases, via direct phosphorylation of p300. Pharmacological or genetic interference with either pathway led to partial assembly of discrete chromatin-bound complexes, which reflected two reversible and distinct cellular phenotypes. Remarkably, PI3K/AKT blockade was permissive for chromatin recruitment of MEF2-SWI/SNF complex, whose remodeling activity was compromised in the absence of MyoD and acetyltransferases. The functional interdependence between p38 and IGF1/PI3K/AKT pathways was further established by the evidence that blockade of AKT chromatin targets was sufficient to prevent the activation of the myogenic program triggered by deliberate activation of p38 signaling.
journal_name
Mol Celljournal_title
Molecular cellauthors
Serra C,Palacios D,Mozzetta C,Forcales SV,Morantte I,Ripani M,Jones DR,Du K,Jhala US,Simone C,Puri PLdoi
10.1016/j.molcel.2007.08.021subject
Has Abstractpub_date
2007-10-26 00:00:00pages
200-13issue
2eissn
1097-2765issn
1097-4164pii
S1097-2765(07)00591-6journal_volume
28pub_type
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