FlyBase Allele Report: Dmel\Past1[110-1]

General Information

Symbol

Dmel\Past1^110-1

Species

D. melanogaster

Name

FlyBase ID

FBal0245167

Feature type

allele

Associated gene

Dmel\Past1

Associated Insertion(s)

Carried in Construct

Key Links

Genomic Maps

JBrowse

Allele class

Mutagen

Delta2-3 transposase

Nature of the Allele

Allele class

Mutagen

Delta2-3 transposase

(Olswang-Kutz et al., 2009)

Progenitor genotype

P{EPgy2}Past1^EY01852

(Olswang-Kutz et al., 2009)

Cytology

Description

Imprecise excision of the progenitor insertion, P{EPgy2}Past1^EY01852, resulting in a 1741 bp deletion.

(Olswang-Kutz et al., 2009)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

deletion

3R:12,697,332..12,699,073 [+]

Comment:

A 1741bp deletion resulting from imprecise excision of P{EPgy2}Past1^EY01852 and extending in both directions from the site of the insertion.

(Olswang-Kutz et al., 2009)

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 developmental rate

(Olswang-Kutz et al., 2009)

abnormal neuroanatomy | third instar larval stage (with Past1^60-4)

(Koles et al., 2015)

abnormal neurophysiology | third instar larval stage (with Past1^60-4)

(Koles et al., 2015)

partially lethal - majority die | heat sensitive

(Olswang-Kutz et al., 2009)

semi-sterile

(Olswang-Kutz et al., 2009)

short lived

(Olswang-Kutz et al., 2009)

Phenotype Manifest In

cone cell | P-stage | increased number

(Dorot et al., 2017)

cystic bulge (with Past1^60-4)

(Olswang-Kutz et al., 2009)

egg chamber

(Olswang-Kutz et al., 2009)

egg chamber (with Past1^60-4)

(Olswang-Kutz et al., 2009)

embryonic/larval garland cell

(Olswang-Kutz et al., 2009)

embryonic/larval neuromuscular junction | third instar larval stage (with Past1^60-4)

(Koles et al., 2015)

individualization stage spermatid (with Past1^60-4)

(Olswang-Kutz et al., 2009)

oocyte

(Olswang-Kutz et al., 2009)

oocyte (with Past1^60-4)

(Olswang-Kutz et al., 2009)

ovary

(Olswang-Kutz et al., 2009)

ovary (with Past1^60-4)

(Olswang-Kutz et al., 2009)

rhabdomere | P-stage

(Dorot et al., 2017)

spermatid cyst (with Past1^60-4)

(Olswang-Kutz et al., 2009)

subsynaptic reticulum | third instar larval stage (with Past1^60-4)

(Koles et al., 2015)

testis (with Past1^60-4)

(Olswang-Kutz et al., 2009)

type I bouton | third instar larval stage (with Past1^60-4)

(Koles et al., 2015)

Detailed Description

Statement

Reference

Past1^110-1 homozygous mutants do not show any external morphological defects in the adult eye but a significant proportion of ommatidia (~40%) in late pupal eyes contain less than seven rhabdomeres and some contain two potential R7 photoreceptors, at early-mid pupal stage the proportion of abnormal ommatidia is about 14%. The abnormal photoreceptor numbers is due to aberrant differentiation of R1/R6 and R7, the differentiation of cone cells is also perturbed as the number of cone cells in early pupa is increased in some ommatidia, but the development of inter-ommatidial pigment cells is not impaired.

(Dorot et al., 2017)

Total bouton numbers (type I) at the neuromuscular junction (NMJ) in Past1^60-4/Past1^110-1 third instar larvae are not significantly different to wild type, but show defects in synaptic bouton shape (less round, often with ragged edges); mutants show a significant increase in ghost boutons (muscle 6/7, segment A3) compared to wild type. Despite reduced GluRIIA levels in Past1^60-4/Past1^110-1 larval NMJs, clusters appose normally to presynaptic active zones.

Past1^60-4/Past1^110-1 larval NMJs show significant reductions in the amplitude and frequency of spontaneous miniature excitatory postsynaptic potentials (mEPSPs) as well as significantly dampened evoked postsynaptic potentials (EPSPs); quantal content is not increased to compensate for reduced mEPSPs (rather, it is significantly decreased).

Subsynaptic reticulum (SSR) in Past1^60-4/Past1^110-1 third instar larval NMJs have a similar recovery rate to wild type after photobleaching boutons, but have a significantly higher mobile fraction (SSR may have reduced complexity in mutants). Mutant 1b boutons show normal presynaptic structures (including synaptic vesicles and active zones) but have aberrant SSR, often separated into distinct nodules with a central core surrounded by long membrane sheets (not seen in wild type).

(Koles et al., 2015)

Past1^110-1 homozygous mutants develop 20% more slowly than heterozygotes. Animals reach adulthood but die three to five days after eclosion, whereas sibling controls survive for over a month.

Past1^110-1 animals are sensitive to high temperatures, and survival is impaired at 29[o]C in larvae and adults.

Fertility is much reduced in Past1^110-1 animals. The number of offspring from Past1^60-4 animals mated with wild-type animals is drastically lower compared to controls.

Past1^60-4/Past1^110-1 males have much thinner testes compared to wildtype. There are significantly fewer bundles of elongating and elongated cysts present. Defects are observed during spermatid individualization, and spermatids fail to extrude their entire cytoplasm into a waste bags.

Ovaries from Past1^60-4/Past1^110-1 or Past1^110-1/Past1^110-1 mated females are much smaller, less organised, and contain few well differentiated oocytes (stages 12-14) compared to ovaries from wildtype or heterozygous mated females. The number of egg chambers is reduced compared to controls.

Past1^110-1 homozygous mutant larval garland cells are defective in endocytosis, and take up much less labelled-avidin compared to controls.

(Olswang-Kutz et al., 2009)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

Past1^110-1 has partially lethal - majority die phenotype, enhanceable by N^nd-1

(Olswang-Kutz et al., 2009)

Past1^110-1 has short lived phenotype, enhanceable by N^nd-1

(Olswang-Kutz et al., 2009)

Other

Statement

Reference

GluRIIA^SP16, Past1^110-1/Past1^60-4 has abnormal neurophysiology | third instar larval stage phenotype

(Koles et al., 2015)

Phenotype Manifest In

Suppressed by

Statement

Reference

Past1^110-1/Past1^60-4 has subsynaptic reticulum | third instar larval stage phenotype, suppressible by Amph²⁶/Amph²⁶

(Koles et al., 2015)

Enhancer of

Statement

Reference

Past1^110-1 is an enhancer of wing phenotype of N^nd-1

(Olswang-Kutz et al., 2009)

Other

Statement

Reference

GluRIIA^SP16, Past1^110-1/Past1^60-4 has embryonic/larval neuromuscular junction | third instar larval stage phenotype

(Koles et al., 2015)

Additional Comments

Genetic Interactions

Statement

Reference

GluRIIA^SP16/GluRIIA^SP16;Past1^60-4/Past1^110-1 double mutant larvae show further reductions in mEPSP amplitude compared to Past1^60-4/Past1^110-1 mutants (but similar in amplitude to GluRIIA^SP16/GluRIIA^SP16 mutants); the compensation increase in quantal content seen in GluRIIA^SP16/GluRIIA^SP16 mutants is not seen in GluRIIA^SP16/GluRIIA^SP16;Past1^60-4/Past1^110-1 double mutants (they show similar diminished quantal content as seen in Past1^60-4/Past1^110-1 larvae).

Amph²⁶/Amph²⁶ suppresses subsynaptic reticulum defects seen at Past1^60-4/Past1^110-1 larval NMJs.

(Koles et al., 2015)

N^nd-1, Past1^110-1 double homozygous flies reach adulthood at a very low frequency, and die after 1 day. The wings are more severely notched compared to N^nd-1 mutant flies.

Only 6% of H², Past1^110-1 double heterozygous mutant flies show defects in wing veins, much reduced compared to single H² mutant flies.

(Olswang-Kutz et al., 2009)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

Past1^110-1 is rescued by Scer\GAL4^GMR.PU/Past1^UAS.B.GFP

(Dorot et al., 2017)

Past1^110-1/Past1^60-4 is rescued by Past1^UAS.EGFP/Scer\GAL4^C57

(Koles et al., 2015)

Comments

Expression of Past1^{Scer\UAS.B.T:Avic\GFP} under the control of Scer\GAL4^GMR.PU almost completely rescues the ommatidial defects (reduced number of rhabdomeres) observed in high proportion of Past1^110-1 homozygous late pupae.

(Dorot et al., 2017)

Expression of Past1^{Scer\UAS.T:Avic\GFP-EGFP} driven in muscles by Scer\GAL4^C57 rescues NMJ morphology and ghost bouton phenotype in Past1^60-4/Past1^110-1 third instar larvae.

(Koles et al., 2015)

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

79616

w^*; sna^Sco/CyO; Past1^110-1/TM6B, Tb¹

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (2)

Reported As

Symbol Synonym

Past1^110-1

(Martin et al., 2024, Dorot et al., 2017, Olswang-Kutz et al., 2009)

past1^110-1

(Koles et al., 2015)

Name Synonyms

Secondary FlyBase IDs

References (4)

Report Sections

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