Loss of cofilin 1 disturbs actin dynamics, adhesion between enveloping and deep cell layers and cell movements during gastrulation in zebrafish.
During gastrulation, cohesive migration drives associated cell layers to the completion of epiboly in zebrafish. The association of different layers relies on E-cadherin based cellular junctions, whose stability can be affected by actin turnover. Here, we examined the effect of malfunctioning actin...
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Public Library of Science (PLoS)
2010-12-01
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| Series: | PLoS ONE |
| Online Access: | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0015331&type=printable |
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| author | Chun-Wei Lin Shuo-Ting Yen Hui-Ting Chang Shiang-Jiuun Chen Shih-Lei Lai Yi-Ching Liu Tun-Hao Chan Wen-Lian Liao Shyh-Jye Lee |
| author_facet | Chun-Wei Lin Shuo-Ting Yen Hui-Ting Chang Shiang-Jiuun Chen Shih-Lei Lai Yi-Ching Liu Tun-Hao Chan Wen-Lian Liao Shyh-Jye Lee |
| author_sort | Chun-Wei Lin |
| collection | DOAJ |
| description | During gastrulation, cohesive migration drives associated cell layers to the completion of epiboly in zebrafish. The association of different layers relies on E-cadherin based cellular junctions, whose stability can be affected by actin turnover. Here, we examined the effect of malfunctioning actin turnover on the epibolic movement by knocking down an actin depolymerizing factor, cofilin 1, using antisense morpholino oligos (MO). Knockdown of cfl1 interfered with epibolic movement of deep cell layer (DEL) but not in the enveloping layer (EVL) and the defect could be specifically rescued by overexpression of cfl1. It appeared that the uncoordinated movements of DEL and EVL were regulated by the differential expression of cfl1 in the DEL, but not EVL as shown by in situ hybridization. The dissociation of DEL and EVL was further evident by the loss of adhesion between layers by using transmission electronic and confocal microscopy analyses. cfl1 morphants also exhibited abnormal convergent extension, cellular migration and actin filaments, but not involution of hypoblast. The cfl1 MO-induced cell migration defect was found to be cell-autonomous in cell transplantation assays. These results suggest that proper actin turnover mediated by Cfl1 is essential for adhesion between DEL and EVL and cell movements during gastrulation in zebrafish. |
| format | Article |
| id | doaj-art-fb388f66d3984f0cb2c9076bcb724fc2 |
| institution | DOAJ |
| issn | 1932-6203 |
| language | English |
| publishDate | 2010-12-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj-art-fb388f66d3984f0cb2c9076bcb724fc22025-08-20T02:48:33ZengPublic Library of Science (PLoS)PLoS ONE1932-62032010-12-01512e1533110.1371/journal.pone.0015331Loss of cofilin 1 disturbs actin dynamics, adhesion between enveloping and deep cell layers and cell movements during gastrulation in zebrafish.Chun-Wei LinShuo-Ting YenHui-Ting ChangShiang-Jiuun ChenShih-Lei LaiYi-Ching LiuTun-Hao ChanWen-Lian LiaoShyh-Jye LeeDuring gastrulation, cohesive migration drives associated cell layers to the completion of epiboly in zebrafish. The association of different layers relies on E-cadherin based cellular junctions, whose stability can be affected by actin turnover. Here, we examined the effect of malfunctioning actin turnover on the epibolic movement by knocking down an actin depolymerizing factor, cofilin 1, using antisense morpholino oligos (MO). Knockdown of cfl1 interfered with epibolic movement of deep cell layer (DEL) but not in the enveloping layer (EVL) and the defect could be specifically rescued by overexpression of cfl1. It appeared that the uncoordinated movements of DEL and EVL were regulated by the differential expression of cfl1 in the DEL, but not EVL as shown by in situ hybridization. The dissociation of DEL and EVL was further evident by the loss of adhesion between layers by using transmission electronic and confocal microscopy analyses. cfl1 morphants also exhibited abnormal convergent extension, cellular migration and actin filaments, but not involution of hypoblast. The cfl1 MO-induced cell migration defect was found to be cell-autonomous in cell transplantation assays. These results suggest that proper actin turnover mediated by Cfl1 is essential for adhesion between DEL and EVL and cell movements during gastrulation in zebrafish.https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0015331&type=printable |
| spellingShingle | Chun-Wei Lin Shuo-Ting Yen Hui-Ting Chang Shiang-Jiuun Chen Shih-Lei Lai Yi-Ching Liu Tun-Hao Chan Wen-Lian Liao Shyh-Jye Lee Loss of cofilin 1 disturbs actin dynamics, adhesion between enveloping and deep cell layers and cell movements during gastrulation in zebrafish. PLoS ONE |
| title | Loss of cofilin 1 disturbs actin dynamics, adhesion between enveloping and deep cell layers and cell movements during gastrulation in zebrafish. |
| title_full | Loss of cofilin 1 disturbs actin dynamics, adhesion between enveloping and deep cell layers and cell movements during gastrulation in zebrafish. |
| title_fullStr | Loss of cofilin 1 disturbs actin dynamics, adhesion between enveloping and deep cell layers and cell movements during gastrulation in zebrafish. |
| title_full_unstemmed | Loss of cofilin 1 disturbs actin dynamics, adhesion between enveloping and deep cell layers and cell movements during gastrulation in zebrafish. |
| title_short | Loss of cofilin 1 disturbs actin dynamics, adhesion between enveloping and deep cell layers and cell movements during gastrulation in zebrafish. |
| title_sort | loss of cofilin 1 disturbs actin dynamics adhesion between enveloping and deep cell layers and cell movements during gastrulation in zebrafish |
| url | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0015331&type=printable |
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