One copy of Dcr-1Q1147X increases the survival rates of both males and female adult flies subjected to nutrient starvation when compared to control flies. The levels of triacylglycerides (TAGs) and glycogen are increased at the beginning of starvation and the consumption of energy resources is delayed with time.
Homozygous Dcr-1Q1147X adult mushroom body clones display a reduction in cell number and absence of α'/β' and α/β neurons.
Homozygous anterodorsal projection neuron (adPN) clones show a reduction in cell number compared to controls when analysed at the adult stage. This cell number defect is not seen in homozygous adPN clones in which only early larval born adPNs are marked.
7 days old females carrying homozygous germline clones result in egg chambers with 8 nurse cells and no oocyte with 37% penetrance.
Wings containing homozygous clones are not flat and show blistering, but there is no loss of margin tissue.
Small homozygous clones in the wing disc contain apoptotic cells.
Dcr-1Q1147X heterozygosity enhances the wing size defects caused by the expression of Scer\GAL4en-e16E>Dcr-1GD11429. The viability of these flies is drastically reduced.
Wing margin cells of Dcr-1Q1147X mutant somatic clones display size defects compared to surrounding tissue.
Wing disc clones of Dcr-1Q1147X mutant cells are on average smaller than their corresponding wild-type twin clones. These clones are frequently fragmented and many clones are eliminated from the wing disc by 96 h after induction. Most Dcr-1Q1147X mutant clones show signs of apoptosis.
When mutant cells are given a relative growth advantage using the Minute technique using RpS32/+ to impair growth of the other cells, Dcr-1Q1147X mutant clones are recovered at the same frequency as wild-type control clones induced 96 h before dissection. However, Dcr-1Q1147X mutant clones are much smaller than the wild-type control clones.
Dcr-1Q1147X mutant wing disc cells in somatic clones display G[]-S cell cycle delay.
Homozygous clones result in wing blistering, external loss of notum bristles and small, rough eyes.
Homozygous clones contribute far less to the adult eye than their wild-type twin spots.
Homozygous clones induced in the eye disc are unable to eliminate Minute heterozygous
cells, in contrast to wild-type clones.
The low cell division index of homozygous female germline stem cell clones does not change under poor food conditions (in contrast to wild-type clones, where the cell division is dramatically reduced under poor food conditions).
Heterozygous females have normal ovary morphology and normal fertility.
Dcr-1Q1147X MARCM clones do not exhibit a significantly reduced number of dendritic ends of ddaC neurons; however, terminal branches fail to elaborate properly.
Homozygous embryos do not develop past the first larval instar stage.
Dcr-1Q1147X mutant germline stem cells (GSCs) that have been generated during adult stages divide slowly compared to wild type, with mutant stem cells producing one progeny compared to 4 in controls. Dcr-1[Q1147X] mutant stem cells often leave the niche; if a wild type stem cell is also present in the niche it divides to replace the missing mutant, but if both of the GSCs present are mutant the niche is left empty. On average 12% of Dcr-1Q1147X mutant GSCs are lost per day, compared to only 2% of control GSCs.
70% of embryos produced by females with Dcr-1Q1147X germline clones are devoid of pole cells and the remaining 32% contain ~16 pole cells. 37% of these embryos are arrested at embryonic cycle 1 or are unfertilized, and 9% are arrested before cycle 8. In addition, these embryos show severe defects in chromosomal segregation, nuclear distribution and supernumerary mitoses. Among mitotically normal embryos from Dcr-1Q1147X mothers with nuclei present in the posterior pole region at cycle 9-14, 50% of them had no pole cells, and 22% contained fewer than ten pole cells.
When Dcr-1Q1147X germline clones are made in the ovarioles, many of the developmental stages are missing in the ovarioles. The proportion of germline stem cells (GSCs) remains close to normal in these clones. Mutant GSCs show normal spectrosome morphology and position. The frequency of cell division in mutant GSCs is reduced to 18% of normal levels. The number of these mutant GSCs that in S phase is also reduced, suggesting that the cell cycle is delayed at the G1/S transition. Affects in the cell cycle are also seen in male germline stem cells.