2015
DOI: 10.1083/jcb.201503006
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PAR-4 and anillin regulate myosin to coordinate spindle and furrow position during asymmetric division

Abstract: PAR-4/LKB-1, PIG-1/MELK, and the anillin ANI-1 inhibit the accumulation of myosin at the anterior cortex of asymmetrically dividing one-cell C. elegans embryos, thereby preventing myosin from uncoupling cytokinetic furrow and mitotic spindle positions.

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Cited by 38 publications
(63 citation statements)
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References 40 publications
(70 reference statements)
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“…Similarly, the first mitosis of C. elegans zygote is also characterized by asymmetric daughter cell sizes (Rose and Gonczy, 2014). Asymmetric spindle morphology contributes to cell size asymmetry together with a myosin-dependent pathway that controls cleavage furrow positioning (Cabernard et al, 2010; Knoblich, 2010; Pacquelet et al, 2015). These examples highlight that the asymmetry in daughter cell sizes can be a programmed process and does not inherently lead to cell death, as observed in klp10A RNAi GSC divisions.…”
Section: Discussionmentioning
confidence: 99%
“…Similarly, the first mitosis of C. elegans zygote is also characterized by asymmetric daughter cell sizes (Rose and Gonczy, 2014). Asymmetric spindle morphology contributes to cell size asymmetry together with a myosin-dependent pathway that controls cleavage furrow positioning (Cabernard et al, 2010; Knoblich, 2010; Pacquelet et al, 2015). These examples highlight that the asymmetry in daughter cell sizes can be a programmed process and does not inherently lead to cell death, as observed in klp10A RNAi GSC divisions.…”
Section: Discussionmentioning
confidence: 99%
“…However, spindle-cortex crosstalk is flexible. Thus, asymmetries in the cortex can bias the site of furrow formation [100][101][102] . In addition, preexisting cortical asymmetries can mod ify the rate of anaphase elongation 101 to alter the size of daughter cells.…”
Section: Spindle Assembly Check Pointmentioning
confidence: 99%
“…Par4 is a homolog of the liver kinase B1 (LKB1) and regulates myosin activity at the aPar and pPar boundary. Par4 controls myosin activity through phosphorylation of anilin, a non-muscle myosin regulator (Chartier et al, 2011b;Pacquelet et al, 2015). Par5 belongs to the family of 14-3-3 regulatory proteins, and binds and inhibits cortical localization of aPars in the posterior of the embryo (Morton et al, 2002).…”
Section: Box 2 Cell Polarity In Birth Defects and Diseasementioning
confidence: 99%