E-Cadherin/HMR-1 Membrane Enrichment Is Polarized by WAVE-Dependent Branched Actin
Polarized epithelial cells adhere to each other at apical junctions that connect to the apical F-actin belt. Regulated remodeling of apical junctions supports morphogenesis, while dysregulated remodeling promotes diseases such as cancer. We have documented that branched actin regulator, WAVE, and ap...
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| Format: | Article |
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MDPI AG
2021-05-01
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| Series: | Journal of Developmental Biology |
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| Online Access: | https://www.mdpi.com/2221-3759/9/2/19 |
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| author | Luigy Cordova-Burgos Falshruti B. Patel Martha C. Soto |
| author_facet | Luigy Cordova-Burgos Falshruti B. Patel Martha C. Soto |
| author_sort | Luigy Cordova-Burgos |
| collection | DOAJ |
| description | Polarized epithelial cells adhere to each other at apical junctions that connect to the apical F-actin belt. Regulated remodeling of apical junctions supports morphogenesis, while dysregulated remodeling promotes diseases such as cancer. We have documented that branched actin regulator, WAVE, and apical junction protein, Cadherin, assemble together in developing <i>C. elegans</i> embryonic junctions. If WAVE is missing in embryonic epithelia, too much Cadherin assembles at apical membranes, and yet apical F-actin is reduced, suggesting the excess Cadherin is not fully functional. We proposed that WAVE supports apical junctions by regulating the dynamic accumulation of Cadherin at membranes. To test this model, here we examine if WAVE is required for Cadherin membrane enrichment and apical–basal polarity in a maturing epithelium, the post-embryonic <i>C. elegans</i> intestine. We find that larval and adult intestines have distinct apicobasal populations of Cadherin, each with distinct dependence on WAVE branched actin. In vivo imaging shows that loss of WAVE components alters post-embryonic E-cadherin membrane enrichment, especially at apicolateral regions, and alters the lateral membrane. Analysis of a biosensor for PI(4,5)P2 suggests loss of WAVE or Cadherin alters the polarity of the epithelial membrane. EM (electron microscopy) illustrates lateral membrane changes including separations. These findings have implications for understanding how mutations in WAVE and Cadherin may alter cell polarity. |
| first_indexed | 2024-03-10T11:38:17Z |
| format | Article |
| id | doaj.art-2192bd4702444623b49e4e1e91e65911 |
| institution | Directory Open Access Journal |
| issn | 2221-3759 |
| language | English |
| last_indexed | 2024-03-10T11:38:17Z |
| publishDate | 2021-05-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Journal of Developmental Biology |
| spelling | doaj.art-2192bd4702444623b49e4e1e91e659112023-11-21T18:39:18ZengMDPI AGJournal of Developmental Biology2221-37592021-05-01921910.3390/jdb9020019E-Cadherin/HMR-1 Membrane Enrichment Is Polarized by WAVE-Dependent Branched ActinLuigy Cordova-Burgos0Falshruti B. Patel1Martha C. Soto2Department of Pathology and Laboratory Medicine, Rutgers—RWJMS, Piscataway, NJ 08854, USADepartment of Pathology and Laboratory Medicine, Rutgers—RWJMS, Piscataway, NJ 08854, USADepartment of Pathology and Laboratory Medicine, Rutgers—RWJMS, Piscataway, NJ 08854, USAPolarized epithelial cells adhere to each other at apical junctions that connect to the apical F-actin belt. Regulated remodeling of apical junctions supports morphogenesis, while dysregulated remodeling promotes diseases such as cancer. We have documented that branched actin regulator, WAVE, and apical junction protein, Cadherin, assemble together in developing <i>C. elegans</i> embryonic junctions. If WAVE is missing in embryonic epithelia, too much Cadherin assembles at apical membranes, and yet apical F-actin is reduced, suggesting the excess Cadherin is not fully functional. We proposed that WAVE supports apical junctions by regulating the dynamic accumulation of Cadherin at membranes. To test this model, here we examine if WAVE is required for Cadherin membrane enrichment and apical–basal polarity in a maturing epithelium, the post-embryonic <i>C. elegans</i> intestine. We find that larval and adult intestines have distinct apicobasal populations of Cadherin, each with distinct dependence on WAVE branched actin. In vivo imaging shows that loss of WAVE components alters post-embryonic E-cadherin membrane enrichment, especially at apicolateral regions, and alters the lateral membrane. Analysis of a biosensor for PI(4,5)P2 suggests loss of WAVE or Cadherin alters the polarity of the epithelial membrane. EM (electron microscopy) illustrates lateral membrane changes including separations. These findings have implications for understanding how mutations in WAVE and Cadherin may alter cell polarity.https://www.mdpi.com/2221-3759/9/2/19epithelial polaritybranched actinCadherinapical junctions |
| spellingShingle | Luigy Cordova-Burgos Falshruti B. Patel Martha C. Soto E-Cadherin/HMR-1 Membrane Enrichment Is Polarized by WAVE-Dependent Branched Actin Journal of Developmental Biology epithelial polarity branched actin Cadherin apical junctions |
| title | E-Cadherin/HMR-1 Membrane Enrichment Is Polarized by WAVE-Dependent Branched Actin |
| title_full | E-Cadherin/HMR-1 Membrane Enrichment Is Polarized by WAVE-Dependent Branched Actin |
| title_fullStr | E-Cadherin/HMR-1 Membrane Enrichment Is Polarized by WAVE-Dependent Branched Actin |
| title_full_unstemmed | E-Cadherin/HMR-1 Membrane Enrichment Is Polarized by WAVE-Dependent Branched Actin |
| title_short | E-Cadherin/HMR-1 Membrane Enrichment Is Polarized by WAVE-Dependent Branched Actin |
| title_sort | e cadherin hmr 1 membrane enrichment is polarized by wave dependent branched actin |
| topic | epithelial polarity branched actin Cadherin apical junctions |
| url | https://www.mdpi.com/2221-3759/9/2/19 |
| work_keys_str_mv | AT luigycordovaburgos ecadherinhmr1membraneenrichmentispolarizedbywavedependentbranchedactin AT falshrutibpatel ecadherinhmr1membraneenrichmentispolarizedbywavedependentbranchedactin AT marthacsoto ecadherinhmr1membraneenrichmentispolarizedbywavedependentbranchedactin |