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General Information
Symbol
Dmel\sensE2
Species
D. melanogaster
Name
FlyBase ID
FBal0098023
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

C13399909T

Reported nucleotide change:

G?A

Amino acid change:

Q240term | sens-PA

Reported amino acid change:

??term

Comment:

The nucleotide change was reported in the context of surrounding sequence but on the negative strand.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

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.

Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

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 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.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
NOT suppressed by
Statement
Reference
Suppressor of
Statement
Reference

sensE2/sens[+] is a suppressor | partially of visible phenotype of mir-9aJ22/mir-9aE39

NOT Suppressor of
Statement
Reference

sensE2/sens[+] is a non-suppressor of increased cell death phenotype of mir-9aJ22

Other
Phenotype Manifest In
Suppressed by
NOT suppressed by
Statement
Reference
Enhancer of
Statement
Reference

sensE2/sens[+] is an enhancer of medial triple row phenotype of sc10-1

sensE2/sens[+] is an enhancer of eo neuron phenotype of sc10-1

sensE2/sens[+] is an enhancer of tormogen cell phenotype of sc10-1

Suppressor of
Statement
Reference

sensE2/sens[+] is a suppressor | partially of wing margin 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

NOT Suppressor of
Statement
Reference

sensE2/sens[+] is a non-suppressor of wing pouch phenotype of mir-9aJ22/mir-9aE39

Other
Additional Comments
Genetic Interactions
Statement
Reference

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 svp1 double mutant embryos have the same number of photoreceptors as wild type, but none of them express Rh5 and an increased number express Rh6.

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.

sensE2/pnrVX4 double heterozygotes show loss of dorsocentral bristles.

sensE2/pnrVX6 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.

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.

Xenogenetic Interactions
Statement
Reference

Expression of BacA\p35Scer\UAS.cHa, under the control of Scer\GAL4tub, in sensE2 clones fails to rescue the wing margin bristle loss.

Complementation and Rescue Data
Rescued by
Partially rescued by

sensE2 is partially rescued by sens1CCg

Not rescued by

sensE2 is not rescued by sens1CCg

sensE2 is not rescued by sens2CCg

sensE2 is not rescued by sens3CCg

Comments

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.

Images (0)
Mutant
Wild-type
Stocks (5)
Notes on Origin
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
References (29)