C22737540T
Q1147term | Dcr-1-PA
Q1147term
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
Amino acid replacement: Q1147term.
chaeta & mesothoracic tergum | somatic clone
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.
Flies homozygous for Dcr-1Q1147X are not viable.
Dcr-119E2/Dcr-1Q1147X and Dcr-118E6/Dcr-1Q1147X results in pharate adults with normal morphology, although some adult escapers are seen.
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.
Expression of Dcr-1VDRC.cUa driven by Scer\GAL4ple.PF in a heterozygous Dcr-1Q1147X genetic background results in dopaminergic neuron loss and climbing defects.
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[[1]]-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.
Dcr-1Q1147X mutants exhibit defects in eye morphology.
Dcr-1Q1147X flies show a modest but significant disruption of the heterochromatic silencing of the P{T1} reporter in line P{T1}T190-177 and of the P{T1(-FRT)} reporter in line P{T1(-FRT)}T190-177.
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.
Dcr-1Q1147X oocytes are ventralised.
Dcr-1Q1147X, wIR.GMR has size defective phenotype, enhanceable by FBXO11Q803R
Dcr-1Q1147X has starvation stress response defective phenotype, suppressible by p53-ns.3'/p53-ns.5'
Dcr-1Q1147X has starvation stress response defective phenotype, suppressible by p53[+]/p53-ns
Dcr-1Q1147X has increased cell death | somatic clone | third instar larval stage phenotype, suppressible by MycUAS.cZa/Scer\GAL4αTub84B.PL
Dcr-1Q1147X, wIR.GMR has eye color defective phenotype, suppressible by FBXO11Q803R
Dcr-1Q1147X has decreased occurrence of cell division | germline clone | oogenesis phenotype, suppressible | partially by dap[+]/dap4
Dcr-1Q1147X is an enhancer of majority die during first instar larval stage phenotype of Gas41f05565
Dcr-1Q1147X is an enhancer of melanotic necrosis | adult stage phenotype of Gas41f05565
Dcr-1Q1147X/Dcr-1[+] is an enhancer of visible phenotype of Scer\GAL4da.G32, Zzzz\CAG99.UAS.Tag:MYC,Tag:FLAG
Dcr-1Q1147X is an enhancer of increased cell death phenotype of Hsap\ATXN3tr.Q61.UAS.Tag:HA, Scer\GAL4GMR.PF
Dcr-1Q1147X, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF is an enhancer of increased cell death phenotype of Hsap\ATXN3tr.Q78.UAS.Tag:HA, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF
Dcr-1Q1147X/Dcr-1[+] is a suppressor | partially of visible phenotype of Scer\GAL4da.G32, Zzzz\CTGrCUG.99.UAS.Tag:MYC,Tag:FLAG
Dcr-1Q1147X is a suppressor | partially | somatic clone of eye color defective phenotype of wmiRNA.GUS.DsRed(T4)
Dcr-1Q1147X is a suppressor | partially of eye color defective phenotype of wIR.GMR
Dcr-1Q1147X is a suppressor of neuroanatomy defective phenotype of Scer\GAL4477, mir-124UAS.cXa
Dcr-1Q1147X, wIR.GMR has size defective phenotype
Dcr-1Q1147X/Dcr-1[+], r2d21 has female sterile phenotype
Dcr-1Q1147X/Dcr-1[+], Dcr-2R416X has female fertile phenotype
Dcr-1Q1147X, Mad12/Mad[+] has decreased cell number | somatic clone | larval stage phenotype
Dcr-1Q1147X, Mad12/Mad[+] has decreased cell number | somatic clone | pupal stage phenotype
Dcr-1Q1147X, Dcr-2L811fsX has decreased cell number | somatic clone | larval stage phenotype
Dcr-1Q1147X, Dcr-2L811fsX has decreased cell number | somatic clone | pupal stage phenotype
Dcr-1Q1147X/Dcr-1[+], Mad12 has decreased cell number | somatic clone | larval stage phenotype
Dcr-1Q1147X, wIR.GMR has eye phenotype, enhanceable by FBXO11Q803R
Dcr-1Q1147X has wing disc | somatic clone | third instar larval stage phenotype, suppressible | partially by MycUAS.cZa/Scer\GAL4αTub84B.PL
Dcr-1Q1147X, wIR.GMR has eye phenotype, suppressible by FBXO11Q803R
Dcr-1Q1147X has germline stem cell | germline clone phenotype, suppressible | partially by dap[+]/dap4
Dcr-1Q1147X has female germline cyst | germline clone | oogenesis phenotype, suppressible | partially by dap[+]/dap4
Dcr-1Q1147X is an enhancer of scutum phenotype of Gas41f05565
Dcr-1Q1147X is an enhancer of scutellum phenotype of Gas41f05565
Dcr-1Q1147X/Dcr-1[+] is an enhancer of tergite phenotype of Scer\GAL4da.G32, Zzzz\CAG99.UAS.Tag:MYC,Tag:FLAG
Dcr-1Q1147X/Dcr-1[+] is an enhancer of egg chamber phenotype of r2d21
Dcr-1Q1147X, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF is an enhancer of eye phenotype of Hsap\ATXN3tr.Q78.UAS.Tag:HA, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF
Dcr-1Q1147X, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF is an enhancer of retina phenotype of Hsap\ATXN3tr.Q78.UAS.Tag:HA, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF
Dcr-1Q1147X is an enhancer of eye phenotype of Hsap\ATXN3tr.Q61.UAS.Tag:HA, Scer\GAL4GMR.PF
Dcr-1Q1147X is an enhancer of retina phenotype of Hsap\ATXN3tr.Q61.UAS.Tag:HA, Scer\GAL4GMR.PF
Dcr-1Q1147X/Dcr-1[+] is a suppressor | partially of tergite phenotype of Scer\GAL4da.G32, Zzzz\CTGrCUG.99.UAS.Tag:MYC,Tag:FLAG
Dcr-1Q1147X is a suppressor | partially | somatic clone of eye phenotype of wmiRNA.GUS.DsRed(T4)
Dcr-1Q1147X is a suppressor | partially of eye phenotype of wIR.GMR
Dcr-1Q1147X/Dcr-1[+] is a suppressor of male germline cell phenotype of maelM391/Df(3L)79E-F
Dcr-1Q1147X is a suppressor of abdominal 1 dorsal multidendritic neuron ddaC phenotype of Scer\GAL4477, mir-124UAS.cXa
Dcr-1Q1147X is a suppressor of dendrite phenotype of Scer\GAL4477, mir-124UAS.cXa
Dcr-1Q1147X is a suppressor of eye phenotype of wIR.GMR
Dcr-1Q1147X is a suppressor of pigment cell phenotype of wIR.GMR
Dcr-1Q1147X/Dcr-1[+] is a non-suppressor of wing phenotype of sdFab-X
Dcr-1Q1147X, wIR.GMR has eye phenotype
Dcr-1Q1147X, Mad12/Mad[+] has female germline stem cell | somatic clone | larval stage phenotype
Dcr-1Q1147X, Mad12/Mad[+] has female germline stem cell | somatic clone | pupal stage phenotype
Dcr-1Q1147X, Dcr-2L811fsX has female germline stem cell | somatic clone | larval stage phenotype
Dcr-1Q1147X, Dcr-2L811fsX has female germline stem cell | somatic clone | pupal stage phenotype
Dcr-1Q1147X/Dcr-1[+], Mad12 has female germline stem cell | somatic clone | larval stage phenotype
Dcr-1Q1147X, wIR.GMR has interommatidial bristle phenotype
Dcr-1Q1147X, wIR.GMR has microchaeta phenotype
Dcr-1Q1147X, wIR.GMR has ommatidium phenotype
The mortality of Gas41f05565 homozygotes as well as the necrotic patches (on scutum, notum and scutellum) observed in the surviving adults is further enhanced by combination with Dcr-1Q1147X.
One copy of p53-ns suppresses the increase in survival rate in response to starvation seen in adult Dcr-1Q1147X/+ mutant flies.
Expression of dmScer\UAS.cZa under the control of Scer\GAL4αTub84B.PL in Dcr-1Q1147X mutant somatic clones completely suppresses cell loss, but clone size is not completely restored.
The lighter colour of wIR.GMR eyes is partially suppressed when eyes are also made homozygous mutant for Dcr-1Q1147X (using the "eyFLP/FRT" system). wIR.GMR, Dcr-1Q1147X are also smaller than wIR.GMR eyes.
wIR.GMR eyes made homozygous for both FBX011Q803R and Dcr-1Q1147X (using the "eyFLP/FRT" system) show a greater suppression of the eye pigmentation phenotype but an enhancement of the small eye phenotype seen in wIR.GMR, Dcr-1Q1147X eyes.
The differentiation defects seen in the testes of maelM391/Df(3L)79E-F males are partially rescued by Dcr-1Q1147X/+.
The female fertility defect seen in r2d21 females is dramatically enhanced by Dcr-1Q1147X/+; the females are completely sterile and the ovaries are severely disorganised with completely fused follicles.
Dcr-2R416X ; Dcr-1Q1147X/+ females have normal ovaries and normal fertility.
Ectopic expression of mir-124Scer\UAS.cXa in homozygous Dcr-1Q1147X ddaC neuron clones (under the control of Scer\GAL4477) does not affect the number of dendritic ends, indicating Dcr-1 suppression of mir-124 function.
Dcr-1Q1147X mutant germline stem cells lacking one copy of Mad12 show clear stem cell maintenance defects when clones are generated during late larval/early pupal stages.
Mad12 mutant germline stem cells lacking one copy of Dcr-1Q1147X show clear stem cell maintenance defects when clones are generated during late larval/early pupal stages.
Dcr-1Q1147X Dcr-2L811fsX double mutants show strong germline stem cell maintenance (GSC) defects when GSC clones are induced during late larval/early pupal stages.
Eye degeneration due to expression of Hsap\ATXN3tr.Q61.Scer\UAS.T:Ivir\HA1 in the eye (under the control of Scer\GAL4GMR.PF) is enhanced in a Dcr-1Q1147X background, resulting in a severely degenerated eye with complete loss of pigmentation.
The wing phenotype of sdFab-X flies is still present in sdFab-X;Dcr-1Q1147X/+ flies.
Embryos from AGO1k08121; Dcr-1Q1147X parents show segment polarity defects, a phenotype not seen in either single mutant. Dcr-2L811fsX; Dcr-1Q1147X double mutants show no segment polarity defects.
When dap4/+ and homozygous Dcr-1Q1147X are combined a partial rescue of the cyst production phenotype seen Dcr-1Q1147X mutants is seen.
Dcr-1Q1147X, wIR.GMR animals have eyes that have reduced pigment, and are also reduced in size. The organisation of ommatidial facets is also disrupted and sensory bristles are missing over the eye surface. Other bristles, which flank the eye surface, are sometimes absent or exhibit hyperplasia.
One of two lines expressing Zzzz\CAG99.Scer\UAS.T:Hsap\MYC,T:Zzzz\FLAG using Scer\GAL4da.G32 show a more severe tergite phenotype in the presence of heterozygous Dcr-1Q1147X than when Zzzz\CAG99.Scer\UAS.T:Hsap\MYC,T:Zzzz\FLAG is expressed alone.
In one of two lines expressing Zzzz\CAGrCUG.99.Scer\UAS.T:Hsap\MYC,T:Zzzz\FLAG using Scer\GAL4da.G32 in the presence of heterozygous Dcr-1Q1147X the proportion of progeny with any tergite-disruption phenotype, and those with a strong phenotype, is significantly reduced compared with flies expressing Zzzz\CAGrCUG.99.Scer\UAS.T:Hsap\MYC,T:Zzzz\FLAG alone.