FlyBase Allele Report: Dmel\Ptp99A[1]

General Information

Symbol

Dmel\Ptp99A¹

Species

D. melanogaster

Name

FlyBase ID

FBal0048918

Feature type

allele

Associated gene

Dmel\Ptp99A

Associated Insertion(s)

Carried in Construct

Key Links

Allele class

Mutagen

Nature of the Allele

Allele class

Mutagen

Progenitor genotype

Cytology

Description

Deletes the entire cytoplasmic protein-tyrosine phosphatase domain.

(Desai et al., 1996)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal neuroanatomy | adult stage (with Df(3R)Ptp99A^R3)

(Kurusu and Zinn, 2008)

viable

(Kurusu and Zinn, 2008)

Phenotype Manifest In

larval abdominal segmental nerve

(Desai et al., 1997)

larval intersegmental nerve

(Desai et al., 1997)

lobe system of adult mushroom body (with Df(3R)Ptp99A^R3)

(Kurusu and Zinn, 2008)

Detailed Description

Statement

Reference

Lar mutants exhibit truncation phenotypes of the ISN. Combining Ptp69D or Ptp99A mutants increases the penetrance and severity of the ISN defects, the ISN pathway is truncated at specific branchpoint positions. Triple mutants lacking Lar, Ptp69D or Ptp99A exhibit much stronger ISN phenotypes than any single or double mutant. Lar, Ptp69D or Ptp99A triple mutants also exhibit fusion bypass phenotype of the SNb axons. Fusion bypass is seldom observed in any genotype in which Ptp69D is wild type. Removal of Ptp99A or Lar produces a 10- to 20- fold increase in the frequency of fusion bypass and an increase in complete stall phenotypes.

(Desai et al., 1997)

Viable and fertile over Df(3R)Ptp99A^R3. Ptp99A¹ homozygotes and Ptp99A¹/Df(3R)Ptp99A^R3 heterozygotes have no detectable CNS, PNS or muscle defects. Increases the penetrance and severity of Ptp69D SNb, SNa and RP mutant phenotypes. This enhanced phenotype is completely rescued by one copy of Ptp69D^+t10.5.

(Desai et al., 1996)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressor of

Statement

Reference

Ptp99A[+]/Ptp99A¹ is a suppressor of abnormal neuroanatomy phenotype of Ptp69D¹

(Desai and Purdy, 2003)

Ptp99A[+]/Ptp99A¹ is a suppressor of abnormal neuroanatomy phenotype of Ptp69D¹⁰

(Desai and Purdy, 2003)

Ptp99A[+]/Ptp99A¹ is a suppressor of abnormal neuroanatomy phenotype of Ptp69D⁷

(Desai and Purdy, 2003)

Other

Statement

Reference

Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp69D¹ has abnormal neuroanatomy | embryonic stage 16 phenotype

(Sun et al., 2001)

Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp10D¹ has abnormal neuroanatomy | embryonic stage 16 phenotype

(Sun et al., 2001)

Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹ has abnormal neuroanatomy | embryonic stage 16 phenotype

(Sun et al., 2001)

Df(3R)Ptp99A^R3/Ptp99A¹, Ptp10D¹, Ptp69D¹ has abnormal neuroanatomy | embryonic stage 16 phenotype

(Sun et al., 2001)

Phenotype Manifest In

Enhancer of

Statement

Reference

Ptp99A¹ is an enhancer of ommatidium phenotype of Scer\GAL4^hs.2sev, nmo^UAS.cUa

(Muñoz-Soriano et al., 2013)

Ptp99A¹ is an enhancer of eye phenotype of Scer\GAL4^hs.2sev, nmo^UAS.cUa

(Muñoz-Soriano et al., 2013)

Ptp99A¹ is an enhancer of ommatidium phenotype of Scer\GAL4^GMR.PU, nmo^UAS.cUa

(Muñoz-Soriano et al., 2013)

Ptp99A¹ is an enhancer of eye phenotype of Scer\GAL4^GMR.PU, nmo^UAS.cUa

(Muñoz-Soriano et al., 2013)

Ptp99A¹ is an enhancer of eye phenotype of Scer\GAL4^hs.2sev, miple1^UAS.Tag:HA

(Muñoz-Soriano et al., 2013)

Ptp99A¹ is an enhancer of ommatidium phenotype of Scer\GAL4^hs.2sev, miple1^UAS.Tag:HA

(Muñoz-Soriano et al., 2013)

Ptp99A¹ is an enhancer of larval abdominal segmental nerve phenotype of Ptp69D¹

(Desai et al., 1996)

Ptp99A¹ is an enhancer of RP neuron & axon phenotype of Ptp69D¹

(Desai et al., 1996)

Ptp99A¹ is an enhancer of larval abdominal segmental nerve phenotype of Ptp69D²

(Desai et al., 1996)

Ptp99A¹ is an enhancer of RP neuron & axon phenotype of Ptp69D²

(Desai et al., 1996)

Ptp99A¹ is an enhancer of larval abdominal segmental nerve phenotype of Ptp69D³

(Desai et al., 1996)

Ptp99A¹ is an enhancer of RP neuron & axon phenotype of Ptp69D³

(Desai et al., 1996)

NOT Enhancer of

Statement

Reference

Ptp99A¹ is a non-enhancer of larval VO2 motor neuron phenotype of Ptp52F^18.3

(Schindelholz et al., 2001)

Ptp99A¹ is a non-enhancer of larval VL3/4 motor neuron phenotype of Ptp52F^18.3

(Schindelholz et al., 2001)

Ptp99A¹ is a non-enhancer of larval VO1 motor neuron phenotype of Ptp52F^18.3

(Schindelholz et al., 2001)

Ptp99A¹ is a non-enhancer of larval RP5 motor neuron phenotype of Ptp52F^18.3

(Schindelholz et al., 2001)

Suppressor of

Statement

Reference

Ptp99A¹ is a suppressor of eye phenotype of Scer\GAL4^GMR.PU, miple1^UAS.Tag:HA

(Muñoz-Soriano et al., 2013)

Ptp99A[+]/Ptp99A¹ is a suppressor of larval intersegmental nerve phenotype of Ptp69D⁷

(Desai and Purdy, 2003)

Ptp99A[+]/Ptp99A¹ is a suppressor of larval intersegmental nerve phenotype of Ptp69D¹

(Desai and Purdy, 2003)

Ptp99A[+]/Ptp99A¹ is a suppressor of larval intersegmental nerve phenotype of Ptp69D¹⁰

(Desai and Purdy, 2003)

NOT Suppressor of

Statement

Reference

Ptp99A¹ is a non-suppressor of larval VO2 motor neuron phenotype of Ptp52F^18.3

(Schindelholz et al., 2001)

Ptp99A¹ is a non-suppressor of larval VL3/4 motor neuron phenotype of Ptp52F^18.3

(Schindelholz et al., 2001)

Ptp99A¹ is a non-suppressor of larval VO1 motor neuron phenotype of Ptp52F^18.3

(Schindelholz et al., 2001)

Ptp99A¹ is a non-suppressor of larval RP5 motor neuron phenotype of Ptp52F^18.3

(Schindelholz et al., 2001)

Other

Statement

Reference

Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp69D¹ has larval intersegmental nerve | embryonic stage phenotype

(Sun et al., 2001)

Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp69D¹ has larval intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype

(Sun et al., 2001)

Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp69D¹ has larval ventral nerve cord | embryonic stage 16 phenotype

(Sun et al., 2001)

Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp10D¹ has larval ventral nerve cord | embryonic stage 16 phenotype

(Sun et al., 2001)

Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp10D¹ has larval segmental nerve branch SNa of A1-7 | embryonic stage 16 phenotype

(Sun et al., 2001)

Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹ has larval intersegmental nerve | embryonic stage phenotype

(Sun et al., 2001)

Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹ has larval ventral nerve cord | embryonic stage 16 phenotype

(Sun et al., 2001)

Df(3R)Ptp99A^R3/Ptp99A¹, Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹ has larval segmental nerve branch SNa of A1-7 | embryonic stage phenotype

(Sun et al., 2001)

Df(3R)Ptp99A^R3/Ptp99A¹, Ptp10D¹, Ptp69D¹ has larval ventral nerve cord | embryonic stage 16 phenotype

(Sun et al., 2001)

Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹/Ptp69D^8ex25, Ptp99A^R3/Ptp99A¹ has larval longitudinal connective phenotype

(Sun et al., 2000)

Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹/Ptp69D^8ex25, Ptp99A^R3/Ptp99A¹ has larval ventral nerve cord commissure phenotype

(Sun et al., 2000)

Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹/Ptp69D^8ex25, Ptp99A^R3/Ptp99A¹ has larval anterior commissure phenotype

(Sun et al., 2000)

Lar^5.5/Lar^13.2, Ptp10D¹, Ptp69D¹/Ptp69D^8ex25, Ptp99A^R3/Ptp99A¹ has larval posterior commissure phenotype

(Sun et al., 2000)

Additional Comments

Genetic Interactions

Statement

Reference

A Ptp99A¹ mutant background significantly enhances the ommatidial rotation phenotype found in Scer\GAL4^hs.2sev>miple1^{Scer\UAS.T:Ivir\HA1} mutants.

A Ptp99A¹ background enhances the ommatidial rotation eye phenotype found upon expression of nmo^Scer\UAS.cUa under the control of Scer\GAL4^hs.2sev.

A Ptp99A¹ mutant background significantly enhances the ommatidial rotation phenotype found in Scer\GAL4^GMR.PU>miple1^{Scer\UAS.T:Ivir\HA1} mutants.

A Ptp99A¹ mutant background suppresses the eye roughness seen in flies expressing miple1^{Scer\UAS.T:Ivir\HA1} under the control of Scer\GAL4^GMR.PU.

(Muñoz-Soriano et al., 2013)

The ISNb bypass phenotype seen in Ptp69D⁷ homozygous embryos is largely suppressed by one copy of Ptp99A¹. The ISNb bypass phenotype seen in Ptp69D¹⁰ homozygous embryos is largely suppressed by one copy of Ptp99A¹. The ISNb bypass phenotype seen in Ptp69D¹/Df(3L)8ex34 embryos is suppressed by one copy of Ptp99A¹.

(Desai and Purdy, 2003)

Lar^5.5/Lar^13.2 Ptp69D¹ Ptp99A¹/Df(3R)Ptp99A^R3 triple mutant embryos show severe motor axon defects. The two inner bundles of the ventral nerve cord are very similar to that of wild-type, but the outer bundle, which develops later, is often discontinuous in late stage 16 triple mutant embryos. In addition, about one third of the ISNb nerves fail to leave the intersegmental nerve at the exit junction and continue to grow out along the common intersegmental nerve pathway in these triple mutant embryos. In most of these bypass hemisegments, only one intersegmental nerve branch is visible, and it is usually thicker than normal.

In Ptp10D¹ Lar^5.5/Lar^13.2 Ptp99A¹/Df(3R)Ptp99A^R3 triple mutant embryos the two inner bundles of the ventral nerve cord are very similar to that of wild-type, but the outer bundle, which develops later, is often discontinuous.

Ptp10D¹ Ptp69D¹ Ptp99A¹/Df(3R)Ptp99A^R3 triple mutant embryos produce a phenotype in which the three longitudinal ventral nerve cord bundles are partially fused and many axons cross the midline.

Approximately half of the SNa nerves fail to bifurcate in Ptp10D¹ Lar^5.5/Lar^13.2 Ptp99A¹/Df(3R)Ptp99A^R3 triple mutant embryos.

Approximately half of the SNa nerves either do not reach the bifurcation point at all or are very thin and wandering in Ptp10D¹ Lar^5.5/Lar^13.2 Ptp69D¹ Ptp99A¹/Df(3R)Ptp99A^R3 quadruple mutant embryos.

Approximately half of the intersegmental nerves terminate at the first lateral branch point position and most of the remainder stop at the second lateral branch point in Lar^5.5/Lar^13.2 Ptp69D¹ Ptp99A¹/Df(3R)Ptp99A^R3 triple mutant embryos.

Only about 15% of the intersegmental nerves terminate at the first lateral branch point position and most of the remainder stop at the second lateral branch point in Ptp10D¹ Lar^5.5/Lar^13.2 Ptp69D¹ Ptp99A¹/Df(3R)Ptp99A^R3 quadruple mutant embryos.

Most of the ventral nerve cord axons abnormally cross the midline and the longitudinal bundles are almost absent in Ptp10D¹ Lar^5.5/Lar^13.2 Ptp69D¹ Ptp99A¹/Df(3R)Ptp99A^R3 quadruple mutant embryos. The longitudinal tracts are depleted of axons and the commissures are completely fused and much thicker than normal. No axons are ever observed to enter the ventrolateral muscle field in the quadruple mutant embryos.

(Sun et al., 2001)

Ptp10D¹; Lar^13.2/Lar^5.5; Ptp69D¹ Ptp99A^R3/Ptp69D^8ex25 Ptp99A¹ quadruple mutants have severely disrupted longitudinal tracts and most axons cross the midline. The bundles that cross the midline do not respect the normal boundaries of the commissures and the anterior and posterior commissures appear fused.