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Dcas supports cell polarization and cell-cell adhesion complexes in development.

Tikhmyanova N, Tulin AV, Roegiers F, Golemis EA - PLoS ONE (2010)

Bottom Line: Loss of Dcas had limited effect on embryonal development.However, we found that Dcas is an important modulator of the severity of the developmental phenotypes of mutations affecting integrins (If and mew) and their downstream effectors Fak56D or Src42A.These results support an important role for Cas proteins in cell-cell adhesion signaling in development.

View Article: PubMed Central - PubMed

Affiliation: Fox Chase Cancer Center, Philadelphia, Pennsylvania, United States of America.

ABSTRACT
Mammalian Cas proteins regulate cell migration, division and survival, and are often deregulated in cancer. However, the presence of four paralogous Cas family members in mammals (BCAR1/p130Cas, EFS/Sin1, NEDD9/HEF1/Cas-L, and CASS4/HEPL) has limited their analysis in development. We deleted the single Drosophila Cas gene, Dcas, to probe the developmental function of Dcas. Loss of Dcas had limited effect on embryonal development. However, we found that Dcas is an important modulator of the severity of the developmental phenotypes of mutations affecting integrins (If and mew) and their downstream effectors Fak56D or Src42A. Strikingly, embryonic lethal Fak56D-Dcas double mutant embryos had extensive cell polarity defects, including mislocalization and reduced expression of E-cadherin. Further genetic analysis established that loss of Dcas modified the embryonal lethal phenotypes of embryos with mutations in E-cadherin (Shg) or its signaling partners p120- and beta-catenin (Arm). These results support an important role for Cas proteins in cell-cell adhesion signaling in development.

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Related in: MedlinePlus

Absence of Dcas induces wing defects in Src42A, If, and mew-deficient flies.A. Dcas1/Dcas1 genotype induces a blister (arrows) phenotype in Src42A heterozygous mutant flies. B. Arrows point to typical wing blisters in wings of the flies of the indicated genotypes. C. Representative genetic cross of two double heterozygous parents (If3 and Dcas1; mewEY09631 and Dcas1) to allow analysis of the viability of resulting progeny. Each row in the graph represents percentage of viable progeny of indicated genotype. Only female progeny were analyzed.
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pone-0012369-g003: Absence of Dcas induces wing defects in Src42A, If, and mew-deficient flies.A. Dcas1/Dcas1 genotype induces a blister (arrows) phenotype in Src42A heterozygous mutant flies. B. Arrows point to typical wing blisters in wings of the flies of the indicated genotypes. C. Representative genetic cross of two double heterozygous parents (If3 and Dcas1; mewEY09631 and Dcas1) to allow analysis of the viability of resulting progeny. Each row in the graph represents percentage of viable progeny of indicated genotype. Only female progeny were analyzed.

Mentions: For data shown, the parental crosses were performed as described in Methods and shown in Figures 2A and 3C. The viable adult progeny of indicated genotypes was collected and compared to phenotypically normal double heterozygous siblings (i.e. Fak56CG1/CyO; Dcas1/TM6B, Ubx, y+) in each of 3 independent experiments.


Dcas supports cell polarization and cell-cell adhesion complexes in development.

Tikhmyanova N, Tulin AV, Roegiers F, Golemis EA - PLoS ONE (2010)

Absence of Dcas induces wing defects in Src42A, If, and mew-deficient flies.A. Dcas1/Dcas1 genotype induces a blister (arrows) phenotype in Src42A heterozygous mutant flies. B. Arrows point to typical wing blisters in wings of the flies of the indicated genotypes. C. Representative genetic cross of two double heterozygous parents (If3 and Dcas1; mewEY09631 and Dcas1) to allow analysis of the viability of resulting progeny. Each row in the graph represents percentage of viable progeny of indicated genotype. Only female progeny were analyzed.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2927436&req=5

pone-0012369-g003: Absence of Dcas induces wing defects in Src42A, If, and mew-deficient flies.A. Dcas1/Dcas1 genotype induces a blister (arrows) phenotype in Src42A heterozygous mutant flies. B. Arrows point to typical wing blisters in wings of the flies of the indicated genotypes. C. Representative genetic cross of two double heterozygous parents (If3 and Dcas1; mewEY09631 and Dcas1) to allow analysis of the viability of resulting progeny. Each row in the graph represents percentage of viable progeny of indicated genotype. Only female progeny were analyzed.
Mentions: For data shown, the parental crosses were performed as described in Methods and shown in Figures 2A and 3C. The viable adult progeny of indicated genotypes was collected and compared to phenotypically normal double heterozygous siblings (i.e. Fak56CG1/CyO; Dcas1/TM6B, Ubx, y+) in each of 3 independent experiments.

Bottom Line: Loss of Dcas had limited effect on embryonal development.However, we found that Dcas is an important modulator of the severity of the developmental phenotypes of mutations affecting integrins (If and mew) and their downstream effectors Fak56D or Src42A.These results support an important role for Cas proteins in cell-cell adhesion signaling in development.

View Article: PubMed Central - PubMed

Affiliation: Fox Chase Cancer Center, Philadelphia, Pennsylvania, United States of America.

ABSTRACT
Mammalian Cas proteins regulate cell migration, division and survival, and are often deregulated in cancer. However, the presence of four paralogous Cas family members in mammals (BCAR1/p130Cas, EFS/Sin1, NEDD9/HEF1/Cas-L, and CASS4/HEPL) has limited their analysis in development. We deleted the single Drosophila Cas gene, Dcas, to probe the developmental function of Dcas. Loss of Dcas had limited effect on embryonal development. However, we found that Dcas is an important modulator of the severity of the developmental phenotypes of mutations affecting integrins (If and mew) and their downstream effectors Fak56D or Src42A. Strikingly, embryonic lethal Fak56D-Dcas double mutant embryos had extensive cell polarity defects, including mislocalization and reduced expression of E-cadherin. Further genetic analysis established that loss of Dcas modified the embryonal lethal phenotypes of embryos with mutations in E-cadherin (Shg) or its signaling partners p120- and beta-catenin (Arm). These results support an important role for Cas proteins in cell-cell adhesion signaling in development.

Show MeSH
Related in: MedlinePlus