HMGN1 is dispensable for myogenesis and adipogenesis

Abstract

Expression of key regulatory and tissue specific proteins necessary for myogenesis and adipogenesis are dependent on functional SWI/SNF enzymes that hydrolyze ATP to remodel chromatin and allow factors access to chromatinized DNA. Functional chromatin structural changes also can be facilitated by the high mobility group-N1 (HMGN1) protein. HMGN1 is a chromatin architectural protein that specifically interacts with nucleosomes and has been shown to facilitate the reversal of repressive chromatin structure, thereby making it more conducive for transcription. To determine if HMGN1 functions in myogenesis or adipogensis, two SWI/SNF-dependent processes, we used RNA interference to created stable cell lines with reduced HMGN1 protein levels and differentiated them along the myogenic and adipogenic pathways. We show that neither myogenesis nor adipogenesis was affected by reduced HMGN1 protein levels. We further demonstrate that HMGN1 levels naturally decrease as a function of contact-mediated cell cycle arrest, thereby explaining the lack of requirement for HMGN1 in these cellular differentiation processes.