Small heat-shock protein HSPB3 promotes myogenesis by regulating the lamin B receptor.
作者： Esti Yeger-Lotem , Laura Mediani , Anat Ben-Zvi , Ina Poser , Giovanna Cenacchi
DOI: 10.1038/S41419-021-03737-1
关键词: Lamin B receptor 、 Lamin 、 Myogenesis 、 Cell biology 、 Myocyte 、 Muscle cell differentiation 、 Chemistry 、 Nucleoplasm 、 Chromatin 、 LMNA
摘要: One of the critical events that regulates muscle cell differentiation is replacement lamin B receptor (LBR)-tether with A/C (LMNA)-tether to remodel transcription and induce differentiation-specific genes. Here, we report localization activity LBR-tether are crucially dependent on muscle-specific chaperone HSPB3 depletion prevents differentiation. We further show binds LBR in nucleoplasm maintains it a dynamic state, thus promoting myogenic genes, including genes extracellular matrix. Remarkably, overexpression alone sufficient two human lines, LHCNM2 cells, rhabdomyosarcoma cells. also mutant R116P-HSPB3 from myopathy patient chromatin alterations fiber disorganization, forms nuclear aggregates immobilize LBR. find unable myoblast instead activates unfolded protein response. propose specialized engaged dysfunctional causes neuromuscular disease by deregulating
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