Cortical forces and CDC-42 control clustering of PAR proteins for C. elegans embryonic polarization

Wang, Shyi-Chyi; Low, Tricia Yu Feng; Gole, Leena; Nishimura, Yukako; Yu, Weimiao; Motegi, Fumio

doi:10.1016/j.mod.2017.04.243

Cited by 2 publications

(7 citation statements)

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“…A 1 : CDC-42-PAR-6-PKC-3 A 2 : PAR-3-PAR-6-PKC-3 P 1 : CHIN-1 P 2 : PAR-1-PAR-2 Given that CDC-42 is essential for PKC-3 to exclude PAR-2 independently of PAR-3 (Rodriguez et al, 2017), we included an inhibitory interaction from A 1 to P 2 [PAR-1-PAR-2] in our model. Two previous reports (Rodriguez et al, 2017;Wang et al, 2017) also proposed that PAR-6 and PKC-3 could associate with either PAR-3 or CDC-42 on the cortex. Because PAR-3 is generally essential to recruit PAR-6 and PKC-3 during polarization (Wang et al, 2017), we include a positive interaction from A 2 to A 1 .…”

Section: Modeling Of Par Polarity In Zygotesmentioning

confidence: 80%

“…Two previous reports (Rodriguez et al, 2017;Wang et al, 2017) also proposed that PAR-6 and PKC-3 could associate with either PAR-3 or CDC-42 on the cortex. Because PAR-3 is generally essential to recruit PAR-6 and PKC-3 during polarization (Wang et al, 2017), we include a positive interaction from A 2 to A 1 . CHIN-1 is excluded from the anterior cortex through an unknown mechanism that relies on PKC-3 (Sailer et al, 2015), and interferes active CDC-42 within the posterior cortical domain (Kumfer et al, 2010;Sailer et al, 2015).…”

Section: Modeling Of Par Polarity In Zygotesmentioning

confidence: 80%

“…In contrast to control zygotes, endogenous PAR-3 was significantly minimized or was undetectable at the anterior cortex , 2E, and S3B), suggesting that the polarized state of PAR-6 might be maintained independently of cortical PAR-3 concentration. PAR-3 has been considered a scaffold that locally recruits PAR-6 and PKC-3 to the active form of CDC-42 (Rodriguez et al, 2017;Wang et al, 2017). Despite the essential functions of PAR-3 in wild-type zygotes, PAR-3 becomes dispensable for the cortical loading of PAR-6 and PKC-3 in zygotes depleted of the Hsp90 co-chaperone CDC-37 (Beers and Kemphues, 2006), suggesting an alternative scaffold for PAR-6 and PKC-3.…”

Section: Cortical Par Patterning By a Combinatorial Network Between The Par Complexes And Chin-1mentioning

confidence: 99%

“…A revised model of PAR polarity in C. elegans zygotes To explain our observations and include findings from recent literatures, we revised the previous models by incorporating two additional PAR species, ] and [CHIN-1], and including several molecular interactions among them (Figures 3A and S4B). PAR-3 recruits PAR-6 and PKC-3 to cortical cluster structures during polarization (Wang et al, 2017). CDC-42 can recruit PAR-6 and PKC-3 to the cortex independently of PAR-3 clusters (Rodriguez et al, 2017;Wang et al, 2017).…”

Section: Modeling Of Par Polarity In Zygotesmentioning

confidence: 99%

“…PAR-3 recruits PAR-6 and PKC-3 to cortical cluster structures during polarization (Wang et al, 2017). CDC-42 can recruit PAR-6 and PKC-3 to the cortex independently of PAR-3 clusters (Rodriguez et al, 2017;Wang et al, 2017). Hence, the anterior cortical domain contains at least two species, and .…”

Section: Modeling Of Par Polarity In Zygotesmentioning

confidence: 99%

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A balance between antagonizing PAR proteins specifies the pattern of asymmetric and symmetric divisions in C. elegans embryogenesis

et al. 2021

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Coordination between cell differentiation and proliferation during development requires the balance between asymmetric and symmetric modes of cell division. However, the cellular intrinsic cue underlying the choice between these two division modes remains elusive. Here, we show evidence in Caenorhabditis elegans that the invariable lineage of the division modes is specified by the balance between antagonizing complexes of partitioning-defective (PAR) proteins. By uncoupling unequal inheritance of PAR proteins from that of fate determinants during cell division, we demonstrate that changes in the balance between PAR-2 and PAR-6 can be sufficient to re-program the division modes from symmetric to asymmetric and vice versa in two daughter cells. The division mode adopted occurs independently of asymmetry in cytoplasmic fate determinants, cell-size asymmetry, and cell-cycle asynchrony between sister cells. We propose that the balance between PAR proteins represents an intrinsic self-organizing cue for the specification of the two division modes during development.

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Section: Modeling Of Par Polarity In Zygotesmentioning

confidence: 80%

Section: Modeling Of Par Polarity In Zygotesmentioning

confidence: 80%

Section: Cortical Par Patterning By a Combinatorial Network Between The Par Complexes And Chin-1mentioning

confidence: 99%

Section: Modeling Of Par Polarity In Zygotesmentioning

confidence: 99%

Section: Modeling Of Par Polarity In Zygotesmentioning

confidence: 99%

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A balance between antagonizing PAR proteins specifies the pattern of asymmetric and symmetric divisions in C. elegans embryogenesis

et al. 2021

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Cell cortex regulation by the planar cell polarity protein Prickle1

Huang

Winklbauer

2022

Journal of Cell Biology

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The planar cell polarity pathway regulates cell polarity, adhesion, and rearrangement. Its cytoplasmic core components Prickle (Pk) and Dishevelled (Dvl) often localize as dense puncta at cell membranes to form antagonizing complexes and establish cell asymmetry. In vertebrates, Pk and Dvl have been implicated in actomyosin cortex regulation, but the mechanism of how these proteins control cell mechanics is unclear. Here we demonstrate that in Xenopus prechordal mesoderm cells, diffusely distributed, cytoplasmic Pk1 up-regulates the F-actin content of the cortex. This counteracts cortex down-regulation by Dvl2. Both factors act upstream of casein kinase II to increase or decrease cortical tension. Thus, cortex modulation by Pk1 and Dvl2 is translated into mechanical force and affects cell migration and rearrangement during radial intercalation in the prechordal mesoderm. Pk1 also forms puncta and plaques, which are associated with localized depletion of cortical F-actin, suggesting opposite roles for diffuse and punctate Pk1.

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Cortical forces and CDC-42 control clustering of PAR proteins for C. elegans embryonic polarization

Cited by 2 publications

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A balance between antagonizing PAR proteins specifies the pattern of asymmetric and symmetric divisions in C. elegans embryogenesis

A balance between antagonizing PAR proteins specifies the pattern of asymmetric and symmetric divisions in C. elegans embryogenesis

Cell cortex regulation by the planar cell polarity protein Prickle1

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