Tropomyosin isoforms have specific effects on the transcriptome of undifferentiated and differentiated B35 neuroblastoma cells

Abstract

Tropomyosins, a family of actin‐associated proteins, bestow actin filaments with distinct biochemical and physical properties which are important for determining cell shape and regulating many cellular processes in eukaryotic cells. Here, we used RNA‐seq to investigate the effect of four tropomyosin isoforms on gene expression in undifferentiated and differentiated rat B35 neuroblastoma cells. In undifferentiated cells, overexpression of tropomyosin isoforms Tpm1.12, Tpm2.1, Tpm3.1, and Tpm4.2 differentially regulates a vast number of genes, clustering into several gene ontology terms. In differentiated cells, tropomyosin overexpression exerts a much weaker influence on overall gene expression. Our findings are particularly compelling because they demonstrate that tropomyosin‐dependent changes are attenuated once the cells are induced to follow a defined path of differentiation. Database Sequence data for public availability are deposited in the European Nucleotide Archive under the accession number PRJEB24136.

Distinct actin–tropomyosin cofilament populations drive the functional diversification of cytoskeletal myosin motor complexes

“…Specifically, cytoskeletal Tpm isoforms have been linked to diseases affecting neurosensory functions, platelet disorders, and cancer (Brettle et al, 2016;Latham et al, 2018;Pleines et al, 2017). Transformation and cancerous growth are frequently accompanied by upregulated production of low molecular weight (LMW) Tpm isoforms, such as Tpm 3.1 and Tpm4.2, and loss of high molecular weight (HMW) Tpm isoforms (Hendricks and Weintraub, 1981;Kabbage et al, 2013;Stefen et al, 2006Stefen et al, , 2018. Thus, over-production of complexes function in the absence of troponin or isofunctional troponin-like proteins and the context of greater Tpm isoform diversity.…”

Cancer Cells in all EMT States Lack Rigidity Sensing Depletion of Different Tumor Suppressors Causes Loss of Rigidity Sensing in Cancer Cells

“…Evidence from RNA sequencing has shown that the levels of many different mRNAs change upon the loss or restoration of rigidity sensing in cells from diverse tissues (Stefen et al, 2018). Thus, there appears to be a major state change upon transformation or the loss of rigidity sensing that results in general changes in cell behaviour such as a decrease in single cell rigidity (Cross et al, 2007; Swaminathan et al, 2011, Coughlin et al, 2013), increased traction forces (Peschetola et al, 2013; Li et al, 2016, Li et al, 2017), and increased mechanical sensitivity (Betof et al, 2015; Berrueta et al, 2018; Takao et al, 2019; Tijore, et al, 2019).…”