Spatial confinement of receptor activity by tyrosine phosphatase during directional cell migration

Zhu, Zhiwen; Chai, Yunpeng; Hu, Huifang; Li, Wei; Li, Wenjun; Dong, Meng‐Qiu; Wu, Jiawei; Wang, Zhixin; Ou, Guangshuo

doi:10.1073/pnas.2003019117

Cited by 3 publications

(2 citation statements)

References 36 publications

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“…Microchannels formed between fiber bundles in ECM often serve as highways for cell migration . As the confinement degree of microchannels has been well reported effective in regulating cell behaviors, , here we would like to emphasize the effect of curved morphology of microchannels. To investigate the potential effects of the curvature on cell motility and morphology, we quantified the parameters of microchannels in clinical tissue biopsies and recapitulated them by using hydrogels in vitro .…”

Section: Resultsmentioning

confidence: 99%

Influence of Curvature on Cell Motility and Morphology during Cancer Migration in Confined Microchannels

Liu,

Zhao,

et al. 2024

ACS Appl. Mater. Interfaces

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Microchannels often serve as highways for cancer migration, and their topology largely determines the migration efficiency. Curvature, a topological parameter in biological systems, has recently been reported to be efficient in guiding cell polarization and migration. Curvature varies widely along curved microchannels, while its influence on cell migration remains elusive. Here, we recapitulated the curved microchannels, as observed in clinical tumor tissues with hydrogels, and studied how cancer cells respond to curvature. We found that cells bend more significantly in a larger curvature and exhibit less spreading as well as lower motility. The underlying mechanism is probably based on the hindrance of the movement of cytoskeletal molecules at the curved microchannel walls. Collectively, our results demonstrated that the accelerated actin retrograde flow rate under local curvature has an effective negative regulation on cell motility and morphology, leading to shortened and bent cell morphologies as well as hampered cell migration efficiency.

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Section: Resultsmentioning

confidence: 99%

Influence of Curvature on Cell Motility and Morphology during Cancer Migration in Confined Microchannels

Liu,

Zhao,

et al. 2024

ACS Appl. Mater. Interfaces

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“…However, whether SRC-1 protein itself is enriched at that EMS/P2 contact relative to other contacts in the four-cell embryo has not been tested. We therefore examined the localization of SRC-1 using a strain with SRC-1 endogenously tagged with GFP (Zhu et al, 2020a; Zhu et al, 2020b). SRC-1::GFP was cortically localized to all cell contacts at the four-cell stage, but was not enriched at the EMS/P2 contact compared to other cell contacts (Fig.…”

Section: Resultsmentioning

confidence: 99%

The Rac1 homolog CED-10 is a component of the MES-1/SRC-1 pathway for asymmetric division of theC. elegansEMS blastomere

Lamb,

Liro,

Myles

et al. 2024

Preprint

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Asymmetric cell division is essential for the creation of cell types with different identities and functions. The EMS blastomere of the four-cellCaenorhabditis elegansembryo undergoes an asymmetric division in response to partially redundant signaling pathways. One pathway involves a Wnt signal emanating from the neighboring P2 cell, while the other pathway is defined by the receptor-like MES-1 protein localized at the EMS/P2 cell contact, and the cytoplasmic kinase SRC-1. In response to these pathways, the EMS nuclear-centrosome complex rotates so that the spindle forms on the anterior-posterior axis; after division, the daughter cell contacting P2 becomes the endodermal precursor cell. Here we identify the Rac1 homolog,CED-10, as a new component of the MES-1/SRC-1 pathway. Loss of CED-10 affects both spindle positioning and endoderm specification. Although MES-1 is still present at the EMS/P2 contact inced-10embryos, SRC-1 dependent phosphorylation is reduced. These and other results suggest that CED-10 acts downstream of MES-1 and upstream or at the level of SRC-1 activity. In addition, we find that the branched actin regulator ARX-2 is enriched at the EMS/P2 cell contact site, in a CED-10 dependent manner. Loss of ARX-2 results in spindle positioning defects, suggesting that CED-10 acts through branched actin to promote the asymmetric division of the EMS cell.

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Actin filament debranching regulates cell polarity during cell migration and asymmetric cell division

Xie

Jiang

Zhu

et al. 2021

Proc. Natl. Acad. Sci. U.S.A.

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The formation of the branched actin networks is essential for cell polarity, but it remains unclear how the debranching activity of actin filaments contributes to this process. Here, we showed that an evolutionarily conserved coronin family protein, the Caenorhabditis elegans POD-1, debranched the Arp2/3-nucleated actin filaments in vitro. By fluorescence live imaging analysis of the endogenous POD-1 protein, we found that POD-1 colocalized with Arp2/3 at the leading edge of the migrating C. elegans neuroblasts. Conditional mutations of POD-1 in neuroblasts caused aberrant actin assembly, disrupted cell polarity, and impaired cell migration. In C. elegans one-cell−stage embryos, POD-1 and Arp2/3, moved together during cell polarity establishment, and inhibition of POD-1 blocked Arp2/3 motility and affected the polarized cortical flow, leading to symmetric segregation of cell fate determinants. Together, these results indicate that F-actin debranching organizes actin network and cell polarity in migrating neuroblasts and asymmetrically dividing embryos.

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Spatial confinement of receptor activity by tyrosine phosphatase during directional cell migration

Cited by 3 publications

References 36 publications

Influence of Curvature on Cell Motility and Morphology during Cancer Migration in Confined Microchannels

Influence of Curvature on Cell Motility and Morphology during Cancer Migration in Confined Microchannels

The Rac1 homolog CED-10 is a component of the MES-1/SRC-1 pathway for asymmetric division of theC. elegansEMS blastomere

Actin filament debranching regulates cell polarity during cell migration and asymmetric cell division

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