A frameshift occurs after codon 1139, and the new reading frame terminates after two codons.
Approximate location of small deletion that causes a frameshift after residue 1139. The new reading frame terminates after two codons.
Adult-generated rhea1 homozygous mutant intestinal stem cell clones have reduced maintenance 7 days and 14 days after clone induction compared to control clones; remaining clones contain fewer cells by day 14.
Junction formation between pairs of VL muscles appears normal.
Mutant embryos are indistinguishable from wild type.
Homozygous clones in the wing produce discrete, round blisters of variable size. These blisters can be located anywhere on the wing. Wing venation is normal. The somatic musculature completely detaches from the epidermis in homozygous embryos. This phenotype is not seen until very late in embryogenesis, suggesting that the muscles may detach from the epidermis when muscle contractions begin. Attachments between the muscles are maintained.
Homozygous clones in the wing produce a blistered phenotype.
CAP49e, rhea1 has abnormal cell number | embryonic stage phenotype
CAP49e, rhea1 has embryonic cardioblast phenotype
rhea1, scb2/scb[+] has embryonic heart cardioblast phenotype
rhea1, sd9 has somatic muscle cell phenotype
rhea1, vgnull has muscle attachment site phenotype
Tigx, rhea1 has muscle attachment site phenotype
At early stages (15), the VL muscles show no significant migration or attachment defects in vgnull; rhea1 double mutant embryos. However, at later stages (16+) several muscles, most prevalently VL1 can be seen detaching from their normal location. This muscle detachment phenotype appears to be solely due to a lack of vg activity as it can be rescued through expression of vgScer\UAS.T:Ivir\HA1 in muscle cells.
The direction of VL1 muscle migration is unaffected in vgnull; rhea1 double mutants.
The development of tendon cells is not affected in vgnull; rhea1 double mutants.
sd9; rhea1 double mutants produce a mild somatic musculature phenotype, but otherwise are indistinguishable from rhea1 mutants.
The muscle detachment phenotype found in vgnull; rhea1 double mutant embryos appears to be solely due to a lack of vg activity as it can be rescued through expression of vgScer\UAS.T:Ivir\HA1 in muscle cells.