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Published on: February 21, 2016
Cell cortex regulation by the planar cell polarity protein Prickle1
Yunyun Huang1, Rudolf Winklbauer1
1Department of Cell and Systems Biology, University of Toronto, Toronto, Ontario, Canada.
This study explores how the protein Prickle1 (Pk1) regulates the actomyosin cortex in Xenopus mesoderm cells. The researchers found that diffuse Pk1 increases cortical F-actin content, while Dvl2 decreases it. Both proteins act upstream of casein kinase II to modulate cortical tension. Pk1's diffuse and punctate forms have opposing effects on F-actin, suggesting that Pk1's localization influences cell mechanics. The study also found that Pk1 and Dvl2 affect cell migration and rearrangement during radial intercalation. These findings provide insights into how planar cell polarity proteins regulate cell polarity and tissue morphogenesis.
Area of Science:
- Cell polarity regulation in developmental biology
- Actomyosin cortex dynamics in Xenopus embryology
Background:
Cell polarity is essential for tissue organization and morphogenesis. The planar cell polarity (PCP) pathway includes proteins like Prickle (Pk) and Dishevelled (Dvl), which are known to regulate cell asymmetry and adhesion. Prior research has shown that Pk and Dvl form antagonizing complexes at cell membranes, influencing cell rearrangement. However, the exact mechanism by which these proteins control actomyosin cortex dynamics remains unclear. In vertebrates, Pk and Dvl have been linked to actomyosin cortex regulation, but the specific roles of Pk1 in modulating cortical tension are not fully understood. This gap motivated the current study to investigate how Pk1 influences the actin cortex in Xenopus mesoderm cells. The study aimed to clarify whether Pk1's diffuse and punctate forms have distinct effects on cortical F-actin and cell mechanics.
Purpose Of The Study:
The study aimed to determine how Prickle1 (Pk1) regulates the actomyosin cortex in Xenopus prechordal mesoderm cells. Specifically, the researchers sought to understand whether Pk1's diffuse and punctate forms have opposing effects on cortical F-actin and cell mechanics. The motivation for this work was to clarify the mechanism by which Pk1 and Dishevelled 2 (Dvl2) modulate cortical tension and influence cell migration during radial intercalation. The study focused on Xenopus mesoderm cells because they undergo extensive cell rearrangement during development. The researchers hypothesized that Pk1 and Dvl2 act upstream of casein kinase II to regulate cortical tension. They also aimed to determine whether Pk1's localization affects localized F-actin depletion and cell behavior. The study sought to provide insights into how PCP proteins control cell mechanics and tissue morphogenesis.
Main Methods:
The researchers used Xenopus prechordal mesoderm cells to investigate the role of Pk1 in actomyosin cortex regulation. They employed live imaging and fluorescence microscopy to track Pk1 localization and cortical F-actin dynamics. The study utilized genetic and pharmacological approaches to manipulate Pk1 and Dvl2 levels in cells. The researchers also used biochemical assays to assess the interaction between Pk1, Dvl2, and casein kinase II. They analyzed cortical tension using traction force microscopy and cell migration assays. The study focused on radial intercalation, a process involving cell rearrangement in the mesoderm. The researchers compared the effects of diffuse and punctate Pk1 on cortical F-actin and cell mechanics. They tested whether Pk1 and Dvl2 regulate cortical tension by modulating casein kinase II activity.
Main Results:
The study found that diffuse cytoplasmic Pk1 increases cortical F-actin content in Xenopus mesoderm cells. This effect counteracts the cortex down-regulation caused by Dvl2. Both Pk1 and Dvl2 act upstream of casein kinase II to modulate cortical tension. The researchers observed that Pk1 up-regulates F-actin, while Dvl2 down-regulates it. Pk1's diffuse form increases cortical tension, whereas Dvl2 decreases it. The study also found that Pk1 forms puncta and plaques, which are associated with localized depletion of cortical F-actin. This suggests that diffuse and punctate Pk1 have opposing roles in cortex regulation. The researchers found that Pk1 and Dvl2 influence cell migration and rearrangement during radial intercalation. These findings indicate that Pk1 and Dvl2 regulate actomyosin cortex dynamics through casein kinase II.
Conclusions:
The authors propose that Pk1 and Dvl2 regulate actomyosin cortex dynamics by modulating casein kinase II activity. The study suggests that diffuse Pk1 increases cortical F-actin content, while Dvl2 decreases it. The findings indicate that Pk1 and Dvl2 act upstream of casein kinase II to control cortical tension. The researchers observed that Pk1's diffuse and punctate forms have opposing effects on cortical F-actin. The study supports the idea that Pk1 and Dvl2 influence cell migration and rearrangement during radial intercalation. The authors suggest that Pk1's localization affects localized F-actin depletion and cell mechanics. The study provides insights into how PCP proteins regulate cell polarity and tissue morphogenesis. The findings highlight the importance of Pk1 and Dvl2 in modulating actomyosin cortex dynamics during development.
Frequently Asked Questions
Pk1 increases cortical F-actin content, counteracting Dvl2's effect of decreasing it.
Both Pk1 and Dvl2 act upstream of casein kinase II to modulate cortical tension.
Diffuse Pk1 increases F-actin, while punctate Pk1 is associated with localized F-actin depletion.
Pk1 modulates actomyosin cortex dynamics, affecting cell migration and rearrangement.
Pk1 and Dvl2 regulate cortical tension, influencing cell behavior during radial intercalation.
The study suggests that Pk1 and Dvl2 act upstream of casein kinase II to control cortex dynamics.
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