[86B1-86B1];[86B3-86B3];
A set of isogenic deficiency stocks created by FLP-induced recombination between FRT-carrying transgenic insertions; molecularly defined deletion endpoints correspond to initial location of the progenitor insertions. Initial set of 519 isogenic deletions provides 56% genome coverage.
The current Exelixis collection at the Bloomington Stock Center differs from the original described in FBrf0175003 : a significant number were shown not to carry a deletion and have been removed from the collection; a number of stocks have been lost; a number of additional deletions are included that were generated after publication.
86B1;86B2
86B1;86B3
Breakpoint from FlyBase's release 5 sequence location of progenitor insertion.
Df(1)CHES-1-like1 ; Df(3R)Exel6157 double mutant embryos show more severe defects in the arrangement of cardial cells compared to either single mutant.
Df(3L)DocA/+ ; Df(3R)Exel6157/+ double heterozygous embryos show defects in the symmetric cell divisions that give rise to the tin-expressing cardial cells that are significantly more severe than the additive effects of each of the two single heterozygotes. Asymmetric cell division defects in "svp" cardiac progenitor cells are not significantly different from the additive effects of each of the two single heterozygotes.
numb3/+ ; Df(3R)Exel6157/+ double heterozygous embryos show asymmetric cell division defects in "svp" cardiac progenitor cells that are significantly more severe than the additive effects of each of the two single heterozygotes. Defects in the symmetric cell divisions that give rise to the tin-expressing cardial cells in the double heterozygotes are not significantly different from the additive effects of each of the two single heterozygotes.
pnrVX6/+ ; Df(3R)Exel6157/+ double heterozygous embryos show asymmetric cell division defects in "svp" cardiac progenitor cells that are not significantly different from the additive effects of each of the two single heterozygotes. Defects in the symmetric cell divisions that give rise to the tin-expressing cardial cells in the double heterozygotes are not significantly different from the additive effects of each of the two single heterozygotes.
poloS025604/+ ; Df(3R)Exel6157/+ double heterozygous embryos show asymmetric cell division defects in "svp" cardiac progenitor cells that are significantly more severe than the additive effects of each of the two single heterozygotes. Defects in the symmetric cell divisions that give rise to the tin-expressing cardial cells are also significantly more severe in the double heterozygotes.
ponP65/+ ; Df(3R)Exel6157/+ double heterozygous embryos show asymmetric cell division defects in "svp" cardiac progenitor cells that are significantly more severe than the additive effects of each of the two single heterozygotes. Defects in the symmetric cell divisions that give rise to the tin-expressing cardial cells in the double heterozygotes are not significantly different from the additive effects of each of the two single heterozygotes.
tin346/+ ; Df(3R)Exel6157/+ double heterozygous embryos show asymmetric cell division defects in "svp" cardiac progenitor cells that are significantly more severe than the additive effects of each of the two single heterozygotes. Defects in the symmetric cell divisions that give rise to the tin-expressing cardial cells are also significantly more severe in the double heterozygotes.
The cardial cells (CCs) are unevenly distributed in mutant embryos: hemisegments having localised increases or decreases in CC number, occasional enlarged CC nuclei and CCs that are misaligned either with other CCs within a hemisegment or with their counterparts across the dorsal midline are seen.
Cell divisions defects underlie the cardiac defects seen in the embryos. Defects in the asymmetric cell division that in wild-type causes the "svp" progenitor cell to give rise to one svp-expressing CC and one svp-expressing pericardial cell (PC) are seen: in some cases the progenitor produces two svp-expressing CCs, while in other cases, it gives rise to two svp-expressing PCs. In other cases karyokinesis defects are seen during the asymmetric division of the "svp" progenitor cell: the posterior-most svp-expressing CC nuclei in each hemisegment are arrested in the process of dividing, and the two nuclei are unable to dissociate. This does not change the number of svp-expressing CCs, but results in a reduction in the number of associated svp-expressing PCs. Karyokinesis defects are also seen in the the symmetrically dividing tin-expressing CCs, resulting in localised reduction in the number of these cells. Additional cell divisions sometimes occur in the tin-expressing CCs.
Limits computationally determined from location of progenitor P insertion on genome sequence between P{EP}Fmr1EP3517/P{PZ}tws02414 and P{PZ}jumu06439/P{lacW}l(3)j8B6j8B6