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  • That disassembling actin filaments transport chromosomes

    2024-06-20

    That disassembling 6-Hydroxydopamine hydrobromide filaments transport chromosomes towards the spindle in oocytes may be surprising at first sight. On the other hand, it is well established that chromosome movement during anaphase is driven by the depolymerization of microtubules [20]. It will be interesting to investigate the similarities and differences in the principles of force generation by depolymerizing microtubules and actin filaments, and to explore the contribution of actin disassembly to force generation in other types of contractile actin networks.
    Introduction Congenital heart defect is one of the highest mortality diseases in human, affects about 1% of newborn children, and accounts for as many as 30% of spontaneous abortions (Vincent et al., 2014). 30% of human congenital heart defects were caused by the malformation of outflow tract (OFT) development (Bruneau, 2008, Sinha et al., 2015). OFT and right ventricle (RV) originate from second heart field (SHF) progenitors (Buckingham et al., 2005, Dyer and Kirby, 2009). Therefore, studying the heart development, especially SHF progenitor development, will provide new insights into deciphering the origins of OFT defects and finding clinically relevant genes. The heart develops from two main sources of cardiac progenitors, the first and second heart fields (FHF and SHF, respectively) (Buckingham et al., 2005, Vincent and Buckingham, 2010). 6-Hydroxydopamine hydrobromide Previous studies have shown that the SHF is a progenitor population located in splanchnic and pharyngeal mesoderm (SpM and PM, respectively) (Dyer and Kirby, 2009, Kelly et al., 2001, Mjaatvedt et al., 2001, Waldo et al., 2001), and contributes to the OFT and RV at the arterial pole, and to the atrial myocardium at the venous pole (Cai et al., 2003, Dyer and Kirby, 2009, Kelly et al., 2001). Insufficient addition of SHF cells to the OFT may compromise OFT lengthening, resulting in defects of ventricular separation and arterial arrangement in human and mice, such as double outlet right ventricle (DORV), transposition of great arteries, persistent truncus arteriosus (PTA) and other abnormal heart development (Dyer and Kirby, 2009, Li et al., 2010, Mesbah et al., 2008, Sinha et al., 2015). Previous studies have identified various transcriptional factors and signaling networks that regulating SHF progenitor proliferation and differentiation (Black, 2007, Rochais et al., 2009). Recently, studies showed that SHF progenitors located in SpM and distal OFT have atypical, apicobasally polarized epithelial characteristics (Francou et al., 2014, Li et al., 2016, Ramsbottom et al., 2014, Sinha et al., 2015, Sinha et al., 2012). Dysregulations of the signaling pathways and transcriptional factors operating in epithelial properties of SHF cells result in OFT shortening, further cause the hypoplasia of OFT and RV, such as PCP signaling pathway (Ramsbottom et al., 2014, Sinha et al., 2015, Sinha et al., 2012), transcriptional factor TBX1 (Francou et al., 2014) and Arid3b (Uribe et al., 2014). However, the deployment of SHF cells, and the regulated cellular and molecular mechanisms still remain to be elucidated. WDR1 (WD-repeat domain 1), the mammalian homolog of AIP1 (actin interacting protein 1) in Drosophila, is a major co-factor of actin depolymerizing factor (ADF)/cofilin that actively disassembles ADF/cofilin-bound actin filaments (F-actin). WDR1 can strongly promote the severing activity of ADF/cofilin by capping the barbed ends of the severed filaments and blocking their re-annealing and elongation, leading to the acceleration of actin disassembly (Ono, 2003). Both ADF/cofilin and WDR1 have been shown to promote actin dynamics in various actin-based processes, including cell migration, cytokinesis, phagocytosis and epidermal planar cell polarity (Chen et al., 2001, Luxenburg et al., 2015, Ono, 2003, Xu et al., 2015, Zhang et al., 2011). Our group has previously shown that WDR1 and ADF/cofilin are both required for adherens junction remodeling in Drosophila eye epithelium (Chu et al., 2012), and for mouse myocardial growth and maintenance (Yuan et al., 2014).