Protein trap insertion line, in-frame.
cher protein knock-down by using slmbαTub67C.vhhGFP4 in a cherCPTI001399 homozygous background results in failure to assemble a hexagonal network during cellularization, and leads to premature rounding and constriction; in addition, there is a delay in ventral furrow invagination during gastrulation. On STED super-resolution microscopy, actin filaments fail to acquire the hexagonal conformation observed in controls and instead localize in a diffuse meshwork that occupies the space separating individual nuclei; actin fibers appear less thick than in controls.
cherCPTI001399 homozygotes are female fertile.
Zzzz\VHHdeGradFP.αTub67C, cherCPTI001399 has actomyosin contractile ring | embryonic stage 5 phenotype, enhanceable by Df(3R)Exel6218/Df(3R)Exel6218
Zzzz\VHHdeGradFP.αTub67C, cherCPTI001399 has filamentous actin | embryonic stage 5 phenotype, enhanceable by Df(3R)Exel6218/Df(3R)Exel6218
Zzzz\VHHdeGradFP.αTub67C, cherCPTI001399 has embryonic epidermis | embryonic stage 5 phenotype, enhanceable by Df(3R)Exel6218/Df(3R)Exel6218
The increased/premature actomyosin constriction observed in Df(3R)Exel6218 homozygous embryos or in cher protein depleted embryos (i.e. cherCPTI001399, slmbαTub67C.vhhGFP4 embryos) is enhanced in the double mutant background.