Nucleotide substitution: G?A.
Amino acid replacement: ??term.
G to A transition at coordinate 3L:13393009 (release 5), resulting in a nonsense mutation.
Stop codon in the middle of the coding sequence.
C13399909T
G?A
Q240term | sens-PA
??term
The nucleotide change was reported in the context of surrounding sequence but on the negative strand.
ommatidium | somatic clone (with sensE1)
In sensE2 clones, R8 photoreceptors are missing in the larval/pupal eye; the ring-like Mi1 axon terminals are also missing from the pupal M9-M10 layers.
Mutant embryos show extensive salivary gland cell death at late stages.
The number of segments containing oenocytes, the number of oenocytes per segment and the total number of oenocytes per embryo are all significantly decreased in sensE2 mutant embryos as compared to controls.
sensE2 homozygous clones in the eye (in which sensScer\UAS.cNa is expressed under the control of Scer\GAL4sca-109-68 which rescues R8 cell differentiation, but is not expressed during the late phase of R8 axon targeting) show targeting defects in the medulla; thicker columns, which likely indicate mistargeting of R8 axons to the M6 layer are seen, as well as columns in which the R7 axon terminated in the M6 layer while the R8 axon crosses into a neighbouring column.
sensE2/+ flies do not show a wing bristle phenotype.
Induction of sensE2 clones in the wing leads to a loss of mechanosensory bristles in the anterior wing margin and loss of the noninnervated bristles of the posterior wing margin.
Sensory precursors within sensE2 clones are able to divide, but there is a delay in their division compared with wild-type precursors. The resulting mutant sensory clusters contain multiple neurons and an occasional sheath cell but lack a socket cell in 98% of cases. This indicates that there is a pIIa-to-pIIb transformation in these clones followed by a sheath-to-neuron transformation later in the lineage.
In sensE2 homozygous somatic clones in the eye disc, photoreceptor R8 differentiates prematurely as a founder R2/R5 cell which then recruits a reduced number of photoreceptors compared to wild-type. In clones in the resulting adult eyes, ommatidia are disrupted, but there are no undifferentiated regions.
Mutant larvae have small salivary glands, about a half to a third of the size of normal salivary glands. IN addition the salivary glands of stage 16 mutant larvae are smaller than stage 13 embryos, suggesting the loss may be progressive. The mutant salivary glands have less cells than wild-type. The salivary placodes appear to be normally specified and a re similar to wild-type placodes in size and cell numbers. IN addition salivary ducts are normal. Cells in the salivary glands undergo ectopic apoptosis from late stage 12 through to stage 14.
When somatic clones of sensE2/sensE1 in the eye are made in a Minute background, normally constructed ommatidia containing photoreceptors mutant for sens can only form if the R8 photoreceptor had at least one functional copy of sens. Large patches of mutant ommatidia are readily recovered in adults. These clones are disorganised and of variable size. The number of ommatidia and the spacing between them is not changed from the surrounding wild-type tissue. However all ommatidia have a striking similarity: they do not contain a discernable R8 or R7 photoreceptors.
Heterozygotes do not show a loss of wing margin phenotype.
Homozygous clones lack bristles, sockets and microchaetae. The phenotype is cell autonomous.
sensE2 has visible | somatic clone phenotype, non-suppressible by Scer\GAL4Eq/phylUAS.Tag:MYC
sensE2 is a suppressor | somatic clone of visible phenotype of Scer\GAL4ap-md544, scUAS.cHa
sensE2/sens[+] is a non-suppressor of increased cell death phenotype of mir-9aJ22
sensE2 has embryonic/larval salivary gland phenotype, suppressible by Scer\GAL4arm.PS/BacA\p35UAS.cHa
sensE2 has embryonic/larval salivary gland phenotype, suppressible by Df(3L)H99
sensE2 has embryonic/larval salivary gland phenotype, suppressible by Df(3L)XR38
sensE2 has embryonic/larval salivary gland phenotype, suppressible by hid05014
sensE1/sensE2 has photoreceptor cell R8 | somatic clone | cell non-autonomous phenotype, suppressible by rox63
sensE2 has adult thorax & microchaeta | somatic clone phenotype, non-suppressible by Scer\GAL4Tub.PU/daUAS.cGa
sensE2 has eo neuron | increased number | somatic clone phenotype, non-suppressible by Scer\GAL4Tub.PU/daUAS.cGa
sensE2 has trichogen cell | somatic clone phenotype, non-suppressible by Scer\GAL4Tub.PU/daUAS.cGa
sensE2 has tormogen cell | somatic clone phenotype, non-suppressible by Scer\GAL4Tub.PU/daUAS.cGa
sensE2 has dorsal row of wing sensilla | somatic clone phenotype, non-suppressible by Scer\GAL4Tub.PU/BacA\p35UAS.cHa
sensE2 has ventral row of wing sensilla | somatic clone phenotype, non-suppressible by Scer\GAL4Tub.PU/BacA\p35UAS.cHa
sensE2 has chaeta | somatic clone phenotype, non-suppressible by Scer\GAL4Eq/phylUAS.Tag:MYC
sensE2/sens[+] is an enhancer of medial row of triple row of wing sensilla phenotype of sc10-1
sensE2/sens[+] is an enhancer of tormogen cell phenotype of sc10-1
sensE2 is an enhancer of photoreceptor neuron | somatic clone phenotype of rho7M43, ru1
sensE2/sens[+] is a suppressor | partially of mechanosensory chaeta | increased number | adult stage phenotype of Rbfox1RNAi.UAS, Scer\GAL4sca-109-68
sensE2/sens[+] is a suppressor | partially of wing margin phenotype of mir-9aJ22/mir-9aE39
sensE2/sens[+] is a suppressor | partially of anterior postalar bristle phenotype of mir-9aJ22/mir-9aE39
sensE2/sens[+] is a suppressor | partially of dorsocentral bristle phenotype of mir-9aJ22/mir-9aE39
sensE2 is a suppressor | somatic clone of adult thorax & macrochaeta phenotype of Scer\GAL4ap-md544, scUAS.cHa
sensE2 is a suppressor | somatic clone of adult thorax & microchaeta phenotype of Scer\GAL4ap-md544, scUAS.cHa
sensE2/sens[+] is a non-suppressor of wing pouch phenotype of mir-9aJ22/mir-9aE39
sensE2, svp1 has Rh5 photoreceptor of Bolwig organ phenotype
sensE2, svp1 has Rh6 photoreceptor of Bolwig organ | increased number phenotype
pnr[+]/pnrVX6, sensE2 has dorsocentral bristle phenotype
pnr[+]/pnrVX4, sensE2 has dorsocentral bristle phenotype
EgfrE1, sensE2 has ommatidium phenotype
EgfrE1, sensE2 has ommatidium | somatic clone phenotype
EgfrE1, sensE2 has eye | somatic clone phenotype
Egfr[+]/EgfrE1, sensE2 has ommatidium | somatic clone phenotype
Egfr[+]/EgfrE1, sensE2 has eye | somatic clone phenotype
Heterozygosity for sensE2 partially suppresses the supernumerary thoracic sensory bristle phenotype of individuals expressing Rbfox1dsRNA.Scer\UAS under the control of Scer\GAL4sca-109-68.
sensE2/+ results in an approximately 35% reduction in the loss of wing margin caused by mir-9aJ22/mir-9aE39. sensE2/+ does not rescue the increased cell death seen in the wing discs of mir-9aJ22/mir-9aE39 animals.
sensE2/+ partially suppresses the formation of ectopic dorsocentral and anterior postalar bristles seen in mir-9aJ22/mir-9aE39 adults.
sc10-1; sensE2/+ flies show a severe loss of stout bristles at the wing margin in comparison to sc10-1 single mutants, which show a small loss of these bristles. At the pupal level the sc10-1; sensE2/+ double mutants are almost completely lacking the neurons that should have developed from the mechanosensory precursors; this is an enhancement of the reduced number of neurons seen in sc10-1 single mutant pupae. The double mutants also show a greater loss of socket cells than the single mutants.
Thoracic clones that express daScer\UAS.cGa, under the control of Scer\GAL4tub, in a sensE2 background results in clones that lack microchaetae. Sensory organ precursors in these clones generate extra neurons but no shaft or socket cells, which is similar to sensE2 single mutant clones.
In rho7M43; ru1; sensE2 triple mutant clones, no photoreceptors differentiate except for a few photoreceptors near the clonal boundary, presumably rescued non-autonomously by neighboring wild-type cell. No rescue of photoreceptor development is seen when these triple mutant clones are made in a rox63 homozygous background. Adult eyes containing sensE2 homozygous somatic clones induced in an EgfrE1/+ background are smaller than wild-type. Within the clone there are reduced numbers of ommatidia, as well as gaps of tissue between ommatidia, a phenotype similar to that seen in EgfrE1 homozygotes.
Expression of phylScer\UAS.T:Hsap\MYC under the control of Scer\GAL4Eq1 fails to rescue external sensory organ formation in homozygous sensE2 clones in the notum.
When Df(3L)H99 (A deficiency that uncovers grim, rpr and W) is combined with sensE2, 93% of salivary glands are normal in size (compared with 0% for sensE2 mutants). The addition of W05014 or Df(3L)XR38 (which removed rpr) partially suppresses this phenotype as well, though the suppression by W05014 is quantitatively and qualitatively weaker than Df(3L)XR38.
Clones of sensE2 in the thorax suppress the extra micro- and macrochaetae produced by expression of scScer\UAS.cHa under the control of Scer\GAL4ap-md544.
Expression of BacA\p35Scer\UAS.cHa, under the control of Scer\GAL4tub, in sensE2 clones fails to rescue the wing margin bristle loss.
Expression of sensg.+t is able to rescue the external sensory organs in adult sensE2 clones, which lose almost all mechanosensory bristles.
Expression of sens1CCg is able to rescue many of the external sensory organs in adult sensE2 clones, which lose almost all mechanosensory bristles.
Expression of sens3CCg is unable to rescue the external sensory organs in adult sensE2 clones, which lose almost all mechanosensory bristles.
Expression of sensg.+t is able to rescue loss of post-orbital bristles in sensE2 clones.
Expression of sens1CCg is able to partially restore the number of post-orbital bristles in sensE2 clones to approximately two-thirds of the wild-type.
Expression of sens3CCg is unable to rescue the loss of post-orbital bristles in adult sensE2 clones.
Expression of sens2CCg is unable to rescue the loss of post-orbital bristles in adult sensE2 clones.
Expression of sensg.+t rescues the lethality of sensE2 homozygous embryos.
Expression of sens1CCg does not rescue the lethality of sensE2 homozygous embryos. However, a significant rescue of PNS development is observed. The rescue is however, not complete, as some of the neurons are lost. In addition, the neurons exhibit differentiation, axon guidance, and fasciculation defects.
Expression of sens3CCg does not rescue the lethality of sensE2 homozygous embryos. sens3CCg also does not rescue the PNS defects associated with sensE2.
Induced on: red1 e1