|Feature type||allele||Associated gene||Dmel\cindr|
|Mutagen||in vitro construct - RNAi, in vitro construct - regulatory fusion|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
|Carried in construct|
|Phenotype Manifest In|
Co-expression of cindr[dsRNA.PC.PD.Scer\UAS] and cindr[dsRNA.Scer\UAS] under the control of Scer\GAL4[GR1] results in a significant increase in the number of binucleate follicle cells compared to control egg chambers. The increase in binucleate follicle cells is accompanied by a significant decrease in the average number of follicle cell intercellular bridges per nucleus.
Expression of cindr[dsRNA.Scer\UAS] under the control of Scer\GAL4 results in a weak border cell migration defect in the egg chamber.
Expression of cindr[dsRNA.Scer\UAS] driven by Scer\GAL4[GMR.PF] results in patterning defect in pupal eyes.
Ubiquitous expression of cindr[dsRNA.Scer\UAS] under the control of Scer\GAL4[tub] leads to embryonic and early larval lethality. Expression of cindr[dsRNA.Scer\UAS] and cindr[dsRNA.PC.PD.Scer\UAS] in the eye for at least 24 hours (under the control of Scer\GAL4[GMR.PF]) does not generate any developmental defects. Initial recruitment of 1[o] cells in Scer\GAL4[GMR.PF]>cindr[dsRNA.PC.PD.Scer\UAS], cindr[dsRNA.Scer\UAS] eyes commences normally and many, though not all, fledgling 1[o] cells successfully encircle a central cone cell quartet. However, these emerging 1[o] cells commonly fail to maintain their niches: 1[o] cells often lose contact with their partners, a loss typically coupled with dissolution of their shared junction. As a result, one proto-1[o] cell is often replaced by another cell to generate a new 1[o] cell. Remarkably, this instability of the 1[o]-1[o] interface continues throughout the stages of interommatidial precursor cell patterning hours after 1[o] cells have normally completed their movements. Expression of cindr[dsRNA.Scer\UAS] in the pupal eye (under the control of Scer\GAL4[GMR.PF]) results in misplacement of cells, misorientation of pattern elements within the ommatidial field, and a variable number of pigment cells. An additional one to two pigment cells surround approximately 16% of Scer\GAL4[GMR.PF]>cindr[dsRNA.Scer\UAS] ommatidia. Patterning of the interommatidial precursor cells is delayed or lost in these flies. Small clonal patches of 1[o] cells expressing cindr[dsRNA.PC.PD.Scer\UAS] and cindr[dsRNA.Scer\UAS] under the control of Scer\GAL4[Scer\FRT.Act5C] are consistently smaller than their wild-type neighbours. Paired cindr[dsRNA.PC.PD.Scer\UAS] 1[o] cells frequently retract, permitting a neighbouring wild-type interommatidial precursor cell direct contact with the central cone cells and often leads to an ectopic third 1[o] cell. Strongly reducing cindr activity (in Scer\GAL4[GMR.PF]>cindr[dsRNA.PC.PD.Scer\UAS], cindr[dsRNA.Scer\UAS] mutants) has a marked effect on F-actin during interommatidial precursor cell patterning: at 28 hours APF, the density of F-actin fibrils and spikes filling the cytoplasm of interommatidial precursor cells is markedly increased. At later stages of patterning, a more dense and disorganized cytoskeletal network is observed in interommatidial precursor cells and the radiating arrangement of actin fibrils in 1[o] cells absent at 41 hours APF. Within cone cells, F-actin levels are mildly elevated at 28 hours APF, and distinct F-actin spikes fail to radiate from cell membranes.
|Phenotype Manifest In|
Expression of cindr[dsRNA.Scer\UAS] under the control of Scer\GAL4 in a mim[null] background restores the ability of border cells in the egg chamber to migrate.
|Complementation & Rescue Data|
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 1 )|
|Secondary FlyBase IDs|
|References ( 4 )|