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General Information
D. melanogaster
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Feature type
Associated gene
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Nature of the Allele
Mutations Mapped to the Genome
Additional Notes
Associated Sequence Data
DNA sequence
Protein sequence
Progenitor genotype
Nature of the lesion
Expression Data
Reporter Expression
Additional Information
Marker for
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Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Modifiers Based on Experimental Evidence ( 1 )
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Disease-implicated variant(s)
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

photoreceptor cell R2 & axon

photoreceptor cell R5 & axon

Detailed Description

Ostia cells of the svp1 homozygote embryos are rounder, losing their characteristic elongated shape.

svp1/svp11C115 mutants exhibit Eya-positive Ap neuron loss in 30% thoracic hemisegments. In the hemisegments in which Ap neurons are generated an increase in Ap neuron number is observed, from 4 to approximately 6 cells. Extra Ap1/Nplp1 neurons are seen and there is loss of the Ap4/FMRFa cell fate.

Homozygous clones in the retina have ommatidia which lack some out photoreceptor cells.

svp1 homozygous mutant animals show a significant increase in the numer of SE2 neurons specified.

svp1 mutants produce the normal number of fully developed and attaching alary muscles. Although occasioanl patterning defects are observed, these are not more prevalent in svp1 mutants than in controls.

Individual svp1 mutant R1 and R6 clone cells (generated using MARCM) terminate in the R8 target layer. When R7 photoreceptors are ablated using sevV1, svp1 mutant R1 and R6 axons terminate in the R7 and R8 layers of the medulla with approximately equal frequency.

50% of svp1 mutant R1 and 53% of R6 clone cells have adopted characteristics usually seen in R8 cells: expression of R8 rhodopsins, small rhabdomeres (rather than the large ones usually seen), and nuclei that are located proximal to R1, R6 and R7 nuclei. A further 42% of svp1 mutant R1s and 41% of R6s have adopted R7 characteristics, having small rhabdomeres that contain R7 rhodopsins. The nuclei are not displaced proximally in these cells. Few R1/R6 cells are seen that express both R7 and R8 rhodopsins, and there is a strong correlation between cells that express R7 or R8 rhodopsins and those that target the equivalent layer of the medulla, indicating that svp1 mutant R1 and R6 cells take on either an R7 or an R8 cell fate, not a mixed fate. None of the mutant R1s and R6s form a regular spatial pattern. svp1 mutant R1/R6 cells are directed towards R7 or R8 fates shortly after their recruitment during larval development.

76% of svp1 mutant R4 clone cells in otherwise wild type ommatidia have small rhabdomeres, rather than the large ones usually seen, and also lack the R1-R6 specific rhodopsin ninaE. Approximately half express R7 rhodopsins and half express R8 rhodopsins.

77% of svp1 mutant R3 clone cells in otherwise wild type ommatidia retain the usual large outer rhabdomere and continue to express the R1-R6 specific rhodopsin ninaE. The remainder adopting R7 or R8 fates with equal likelihood. A similar R7/R8 conversion is seen in svp1 mutant mystery cells. The mutant R3s with large outer rhabdomeres are in ommatidia with reversed chirality, indicating that they have adopted an R4 cell fate.

Eyes wholly mutant for svp1 (generated using WGMR.PG) contain increased numbers of R7 and R8 cells (2.2 and 2.5 per ommatidium respectively).

The total number of photoreceptor cells in the Bolwig's organ of mutant embryos is normal. However, all the photoreceptors are of the Rh5-positive subtype and no Rh6-positive photoreceptors are seen.

svp1 mutants exhibit a reduction in the number of NB6-4T-derived neurons in almost all hemineuromeres.

Photoreceptor cells R3, R4, R1 and R6 are transformed into R7 cells.

svp1/svp2 embryos have extra U1 neurons at the expense of later born U neurons from the same (NB7-1) lineage. U4 and U5 neurons are particularly depleted. Similarly, there are increased numbers of early born cells from the NB 7-3 lineage (EW1 and GW) compared to later born cells from this lineage.

In homozygous clones in the eye, most ommatidia have three to five cells with small rhabdomeres.

svp1 mutant embryos have an estimated 90 cells in each Malpighian tubule cell (as opposed to about 125 in wild-type).

R1, R3, R4 and R6 are transformed to R7 cells. Targets chosen by R2 and R5 are invariably misorientated with respect to the equator.

Mosaic ommatidia at the border of homozygous clones in the eye show polarity defects, including misrotations, wrong chirality or symmetrical, non-chiral ommatidia. When one cell of the R3/R4 pair is mutant in mosaic ommatidia, the ommatidium adopts the wrong chiral form and the svp- cell assumes the R4 position. Mosaic ommatidia with mutant R1 or R6 cells behave normally. Misrotated R3/R4 precursor pairs are seen in homozygous clones in the third larval instar eye disc. These cells are misrotated by approximately 45o or 90o from their normally oriented neighbours.

Homozygous embryos have a reduced number of cells in both the anterior and posterior Malpighian tubules compared to wild-type embryos. Tip cell determination occurs normally in these embryos. BrdU incorporation appears relatively normal during the initial cell divisions of the Malpighian tubules, but subsequently it is strongly reduced indicating a failure of DNA replication.

In svp mutant clones the R1 and R6 cells are missing.

embryonic lethal

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Suppressor of

svp1 is a suppressor of lethal | recessive phenotype of kay2

Phenotype Manifest In
Enhanced by

svp2/svp1 has EW2 neuron phenotype, enhanceable by KrmCD, Kr1/Kr1

svp2/svp1 has EW3 neuron phenotype, enhanceable by KrmCD, Kr1/Kr1

svp2/svp1 has U4 neuron phenotype, enhanceable by KrmCD, Kr1/Kr1

svp2/svp1 has U5 neuron phenotype, enhanceable by KrmCD, Kr1/Kr1

Suppressed by

Kr1, KrmCD, svp2/svp1 has EW3 neuron phenotype, suppressible | partially by hb15/hb12

Kr1, KrmCD, svp2/svp1 has U4 neuron phenotype, suppressible | partially by hb15/hb12

Kr1, KrmCD, svp2/svp1 has U5 neuron phenotype, suppressible | partially by hb15/hb12

Enhancer of
Suppressor of

svp1 is a suppressor of embryo | dorsal closure stage phenotype of kay1/kay2

Additional Comments
Genetic Interactions

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.

Nact.sev expression in svp1 mutant R1/R6 cells (generated using WGMR.PG) results in all cells transforming to a R7 cell fate, as opposed to either an R7 or R8 fate as is seen in cells that are only mutant for svp1.

KrmCD; Kr1/Kr1 enhances the reduction in later born neurons of the NB7-1 an NB2-3 lineages see in svp1/svp2 embryos so that U4 and U5 are almost completely eliminated, as are EW2 and EW3. This enhanced phenotype is partially suppressed if the embryos are also hb12/hb15.

svp1 Df(2L)32FP-5 double mutant ommatidia have the same phenotype as Df(2L)32FP-5 single mutant ommatidia in clones in the eye; small rhabdomeres are not seen.

kay2/kay2 svp1 flies are viable, and sometimes have mild thorax closure defects. tll1 svp1 double mutant clones in the wing show formation of ectopic vein tissue. This phenotype is approximately 100% penetrant and is cell autonomous.

Double mutant clones with rox63, in otherwise wild type ommatidia, contain only central type receptor cells. The overall number of photoreceptor cells in each ommatidium is the same in svp-,ro- and svp+,ro- clones.

Xenogenetic Interactions

svp1 dominantly enhances the rough eye phenotype caused by expression of Zzzz\CTGi480.Scer\UAS.cGa under the control of Scer\GAL4sev.PU.

Complementation and Rescue Data
Images (0)
Stocks (2)
Notes on Origin

No interaction with P{sev-svp1} or P{sev-svp2} exists.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (9)
References (48)