Imprecise excision of the P{EP} element, resulting in an 848bp deletion which removes all residues between the P{EP}nocEP2173 insertion site and the noc transcription start site, as well as 330bp of the noc 5'UTR.
Homozygous nocd64 clones develop without any observable defect.
Somatic clones of nocd64 homozygous cells in adult wings or legs have no obvious phenotype.
Homozygous embryos have fewer cells than normal in the lateral anterior trunk and ganglionic branch and lateral branch fusion is occasionally missing. All dorsal branches are formed, but some branches have only up to 3 cells. The terminal cells appear to be duplicated at the expense of the fusion cells in the dorsal branches.
elB3.3.1, nocd64 has neoplasia | adult stage phenotype, suppressible by Scer\GAL4FRT.Act5C/NRNAi.P.UAS
elB3.3.1, nocd64 has neoplasia | adult stage phenotype, suppressible by Scer\GAL4FRT.Act5C/mamN.UAS
elB3.3.1, nocd64 has increased cell number phenotype, suppressible by Scer\GAL4FRT.Act5C/NRNAi.P.UAS
elB3.3.1, nocd64 has increased cell number phenotype, suppressible by Scer\GAL4FRT.Act5C/mamN.UAS
elB3.3.1, nocd64 has increased cell number phenotype, non-suppressible by domeΔCYT.UAS/Scer\GAL4FRT.Act5C
elB3.3.1, nocd64 has neoplasia | adult stage phenotype, non-suppressible by domeΔCYT.UAS/Scer\GAL4FRT.Act5C
elB3.3.1, nocd64 has increased occurrence of cell division | adult stage phenotype
elB3.3.1, nocd64 has neoplasia | adult stage phenotype
elB3.3.1, nocd64 has increased cell number phenotype
elB3.3.1, nocd64 has abnormal cell growth | somatic clone | cell non-autonomous phenotype
elB3.3.1, nocd64 has partially lethal - majority die | somatic clone | pupal stage phenotype
elB3.3.1, nocd64 has eye-antennal disc | somatic clone phenotype, suppressible by Scer\GAL4FRT.Act5C/NRNAi.P.UAS
elB3.3.1, nocd64 has adult head capsule | somatic clone phenotype, suppressible by Scer\GAL4FRT.Act5C/NRNAi.P.UAS
elB3.3.1, nocd64 has eye-antennal disc | somatic clone phenotype, suppressible by Scer\GAL4FRT.Act5C/mamN.UAS
elB3.3.1, nocd64 has adult head capsule | somatic clone phenotype, suppressible by Scer\GAL4FRT.Act5C/mamN.UAS
elB3.3.1, nocd64 has eye-antennal disc | somatic clone phenotype, non-suppressible by domeΔCYT.UAS/Scer\GAL4FRT.Act5C
elB3.3.1, nocd64 has adult head capsule | somatic clone phenotype, non-suppressible by domeΔCYT.UAS/Scer\GAL4FRT.Act5C
elB3.3.1, nocd64 has dorsal margin photoreceptor cell | somatic clone phenotype
elB3.3.1, nocd64 has eye-antennal disc | somatic clone phenotype
elB3.3.1, nocd64 has adult head capsule | somatic clone phenotype
elB3.3.1, nocd64 has wing | somatic clone phenotype
elB3.3.1, nocd64 has coxa | somatic clone phenotype
elB3.3.1, nocd64 has wing disc | distal | somatic clone phenotype
elB3.3.1, nocd64 has trochanter | somatic clone phenotype
elB3.3.1, nocd64 has leg disc | distal | somatic clone phenotype
elB3.3.1, nocd64 has wing hinge | somatic clone phenotype
elB3.3.1, nocd64 has femur | somatic clone phenotype
elB3.3.1, nocd64 has tibia | somatic clone phenotype
elB3.3.1, nocd64 has tarsal segment | somatic clone phenotype
elB3.3.1 nocd64 double mutant ey clones do not show any overt phenotype in the adult antenna or in the most doral or ventral side of the head capsule. When located close to the DV boundary, clones induced overgrowths of the head capsule. The overgrowths are associated with ectopic bristles and consist mainly of mutant cells. However, in some cases, a few wild-type cells are detected in the outgrowths. Clones located in the presumptive antenna appendage or differentiating eye tissue do not show any apparent phenotype in terms of growth effects. When located in the region anterior to the morphogentic furrow, where their expression levels are higher, they caused tissue outgrowth. Mutant cells have a growth advantage over wild-type tissue since clones generating the outgrowths are much larger than those located elsewhere in the eye-antenna disc. Cell size is not affected. All overgrown tissues show increased proliferation. These local elevations are restricted to mutant cells. There is no increase in mitotic activity. There is not apparent accumulation of dying cells compared to wild-type surroundings. When a growth advantage is introduced by means of kiling the twin clones resulting from the FRT-mediated recombination, the extend and frequency of the overgrowths are even greater. These overgrowths very often include ectopic antennae and eye structures. In some cases, multiple ectopic antennae or eyes are detected within the overgrowths. Endogenous antennae and eyes are not affected.
A reduction of N protein levels in elB3.3.1 nocd64 double mutant ey clones, through expression of NdsRNA.P.Scer\UAS under the control of Scer\GAL4Scer\FRT.Act5C reduces the frequency of overgrowths per adult fly from 51.5% to 2.2%, without affecting cell viability.
A reduction of mam protein levels in elB3.3.1 nocd64 double mutant ey clones, through expression of mamN.Scer\UAS under the control of Scer\GAL4Scer\FRT.Act5C reduces the frequency of overgrowths per adult fly from 51.5% to 4.8%, without affecting cell viability.
The frequency of overgrowths observed in elB3.3.1 nocd64 double mutant ey clones is not affected when the JAK-STAT pathway is blocked by expression of dominant-negative domeΔCYT.Scer\UAS (under the control of Scer\GAL4Scer\FRT.Act5C).
elB3.3.1; nocd64 double homozygous somatic clones located distally in the theird instar leg or wing discs are recovered at much lower frequencies than wild-type twin spot clones. Those that are recovered are rounded-up and appear to extrude from the disc epithelium. In contrast, these clones are recovered at the same frequency as their wild-type twin-spots in the proximal regions of wing and leg discs. In adult wings, clones are sometimes recovered as vesicles of mutant tissue between the wing surfaces. Few larvae with many large elB3.3.1; nocd64 double mutant 'minute+' clones in a 'minute-/+' background survive to adulthood. Those that do have legs lacking distal elements (coxa, trochanter, femur, tibia, and tarsal segments) and exhibit an almost complete loss adult wing tissue, with the remaining tissue being heterozygous. These clones cause no obvious adult phenotype when they fall in the notum. When induced in early 3rd instar, these clones lead to loss of wing hinge, non-autonomous reductions in wing size, failure of leg segmentation and loss of trochanter.