|Feature type||allele||Associated gene||Dmel\sens|
|Allele class||amorphic allele - genetic evidence, loss of function allele|
What does this section display?
This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms).
What does this section not display?
This section does not currently display links that were removed or gene model changes.
Click the icon below to subscribe to this FlyBase record and receive updates automatically through your feed reader.
|All updates||Click here to see a list of all updates to this record from FB2010_08 and on.|
|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Amino acid replacement: ??@.
G to A transition at coordinate 3L:13393009 (release 5), resulting in a nonsense mutation.
Nucleotide substitution: G?A.
Stop codon in the middle of the coding sequence.
|Phenotype Manifest In|
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 sens[E2] mutant embryos as compared to controls.
sens[E2] homozygous clones in the eye (in which sens[Scer\UAS.cNa] is expressed under the control of Scer\GAL4[sca-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 mutant clones lose almost all mechanosensory bristles. The number of post-orbital bristles in sensE2 mutant clones is less than a third of the wild-type number.
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.
|NOT suppressed by|
|NOT Suppressor of|
|Phenotype Manifest In|
sensE1/sensE2 has photoreceptor cell R8 | somatic clone | cell non-autonomous phenotype, suppressible by rox63
|NOT suppressed by|
sensE2 has adult thorax & microchaeta | somatic clone phenotype, non-suppressible by Scer\GAL4tub.PU/daScer\UAS.cGa
sensE2 has chaeta | somatic clone phenotype, non-suppressible by Scer\GAL4Eq1/phylScer\UAS.T:Hsap\MYC
sensE2 has dorsal row | somatic clone phenotype, non-suppressible by Scer\GAL4tub.PU/BacA\p35Scer\UAS.cHa
sensE2 has eo neuron | supernumerary | somatic clone phenotype, non-suppressible by Scer\GAL4tub.PU/daScer\UAS.cGa
sensE2 has tormogen cell | somatic clone phenotype, non-suppressible by Scer\GAL4tub.PU/daScer\UAS.cGa
sensE2 has trichogen cell | somatic clone phenotype, non-suppressible by Scer\GAL4tub.PU/daScer\UAS.cGa
sensE2/sens[+] is a suppressor | partially of anterior postalar bristle phenotype of mir-9aJ22/mir-9aE39
sensE2 is a suppressor | somatic clone of adult thorax & macrochaeta phenotype of Scer\GAL4ap-md544, scScer\UAS.cHa
|NOT Suppressor of|
sens[E2]/+ results in an approximately 35% reduction in the loss of wing margin caused by mir-9a[J22]/mir-9a[E39]. sens[E2]/+ does not rescue the increased cell death seen in the wing discs of mir-9a[J22]/mir-9a[E39] animals. sens[E2]/+ partially suppresses the formation of ectopic dorsocentral and anterior postalar bristles seen in mir-9a[J22]/mir-9a[E39] adults.
sens[E2]/pnr[VX4] double heterozygotes show loss of dorsocentral bristles. sens[E2]/pnr[VX6] double heterozygotes show loss of dorsocentral bristles.
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.
The addition of rox63 suppresses the photoreceptor cell R8 phenotype seen in sensE2/sensE1 somatic clones.
|Complementation & Rescue Data|
|Fails to complement|
|Partially rescued by|
|Not rescued by|
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.
|Stocks ( 4 )|
|Notes on Origin|
Induced on: red1 e1
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 5 )|
|Secondary FlyBase IDs|
|References ( 20 )|
|Personal communication to FlyBase|