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Nexilin, encoded by the  NEXN  gene, is expressed in striated muscle and localizes to Z-discs, influencing mechanical stability. We examined Nexilin/ NEXN  in smooth muscle cells (SMCs), and addressed if Nexilin localizes to dense bodies and dense bands and whether it is regulated by actin-controlled coactivators from the MRTF ( MYOCD ,  MKL1 ,  MKL2 ) and YAP/TAZ ( YAP1  and  WWTR1 ) families.  NEXN  expression in SMCs was comparable to that in striated muscles. Immunofluorescence and immunoelectron microscopy suggested that Nexilin localizes to dense bodies and dense bands. Correlations at the mRNA level suggested that  NEXN  expression might be controlled by actin polymerization. Depolymerization of actin using Latrunculin B repressed the  NEXN  mRNA and protein in bladder and coronary artery SMCs. Overexpression and knockdown supported involvement of both YAP/TAZ and MRTFs in the transcriptional control of  NEXN . YAP/TAZ and MRTFs appeared equally important in bladder SMCs, whereas MRTFs dominated in vascular SMCs. Expression of  NEXN  was moreover reduced in situations of SMC phenotypic modulation  in vivo . The proximal promoter of  NEXN  conferred control by MRTF-A/ MKL1  and  MYOCD .  NEXN  silencing reduced actin polymerization and cell migration, as well as SMC marker expression.  NEXN  targeting by actin-controlled coactivators thus amplifies SMC differentiation through the actin cytoskeleton, probably via dense bodies and dense bands.

Nexilin/NEXN controls actin polymerization in smooth muscle and is regulated by myocardin family coactivators and YAP