FlyBase Allele Report: Dmel\Myo31DF[L152]

General Information

Symbol

Dmel\Myo31DF^L152

Species

D. melanogaster

Name

FlyBase ID

FBal0195152

Feature type

allele

Associated gene

Dmel\Myo31DF

Associated Insertion(s)

Carried in Construct

Key Links

Genomic Maps

JBrowse

Allele class

amorphic allele - genetic evidence

loss of function allele

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

amorphic allele - genetic evidence

(Taniguchi et al., 2007)

loss of function allele

(Hozumi et al., 2006)

Mutagen

ethyl methanesulfonate

(Taniguchi et al., 2007, Hozumi et al., 2006)

Progenitor genotype

Cytology

Description

Amino acid replacement: Q331term.

(Hozumi et al., 2006)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

2L:10,494,659..10,494,659 [-]

Nucleotide change:

C10494659T

Amino acid change:

Q331term | Myo31DF-PA; Q331term | Myo31DF-PB; Q331term | Myo31DF-PC

Reported amino acid change:

Q331term

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

(Hozumi et al., 2006)

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 axis specification

(Okumura et al., 2015)

abnormal cell shape | embryonic stage

(Hatori et al., 2014)

fertile

(Taniguchi et al., 2007, Hozumi et al., 2006)

viable

(Taniguchi et al., 2007, Hozumi et al., 2006)

Phenotype Manifest In

Detailed Description

Statement

Reference

The hatching rates and survival rates from first instar larvae to adult of homozygous Myo31DF^L152 mutants (derived from homozygous Myo31DF^L152 mutant females) are similar to those of wild type.

The posterior midgut and hindgut exhibit a left/right (l/r) reversed phenotype in ~80% of the Myo31DF^L152 homozygotes.

(Okumura et al., 2015)

Embryos homozygous for Myo31DF^L152 display inverse left-right asymmetry in the hindgut positioning compared to wild-type. The hindgut epithelial cells in Myo31DF^L152 mutants display predominantly sinistral chirality (more apical cell boundaries fall into the 90[o] to 0[o] angle bin) rather than the dextral chirality predominant in wild type (where most apical cell boundaries fall into the -90[o] to 0[o] angle bin).

(Hatori et al., 2014)

Homozygous embryos show defects in the left-right asymmetry of the hindgut: left-right inversion and (rarely) bilateralism phenotypes are seen at stage 14 in the mutant embryos.

The mean length of the cell boundaries at the apical hindgut epithelium is greater than normal in mutant embryos at late stage 12, early stage 13 and late stage 13.

(Taniguchi et al., 2011)

Mutant hindgut epithelial cells show a reversal of the left-right asymmetric polarity which is seen in wild-type hindgut epithelial cells at late stage 12 (before epithelial tube rotation).

(Taniguchi et al., 2011)

Myo31DF^L152 mutants exhibit approximately 80% left-right symmetry inversion in the midgut and hindgut simultaneously. In contrast, the foregut of Myo31DF^L152 mutant embryos show normal handedness, indicating that these left-right defects are heterotaxic. In addition, in adult Myo31DF^L152 mutant flies, the laterality of the testis and hindgut is reversed.

(Taniguchi et al., 2007)

82.0% of homozygous embryos show inversion of the normal left-right asymmetry of the midgut and hindgut.

Myo31DF^L152/Df(2L)J2 embryos show inversion of the normal left-right asymmetry of the midgut and hindgut (57.7% and 61.5% respectively).

The normal left-right asymmetry of the hindgut is inversed in 85.7% of homozygous adults, while in 2.9% of cases the hindgut is deformed. The handedness of the spiral of the testis is reversed in 78.7% of homozygous males, while in 19.1% of cases the testis is deformed.

(Hozumi et al., 2006)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

Myo31DF^L152 has abnormal axis specification phenotype, enhanceable by Scer\GAL4^da.PU/Myo61F^UAS.cHa

(Okumura et al., 2015)

NOT Enhanced by

Statement

Reference

Myo31DF^L152 has abnormal axis specification phenotype, non-enhanceable by Myo61F¹

(Okumura et al., 2015)

Myo31DF^L152 has abnormal axis specification phenotype, non-enhanceable by Scer\GAL4^da.PU/Myo95E^UAS.D

(Okumura et al., 2015)

Myo31DF^L152 has abnormal axis specification phenotype, non-enhanceable by Myo95E¹

(Okumura et al., 2015)

Myo31DF^L152 has abnormal axis specification phenotype, non-enhanceable by Myo61F¹/Myo95E¹

(Okumura et al., 2015)

Myo31DF^L152 has abnormal axis specification phenotype, non-enhanceable by Scer\GAL4^da.PU/Myo95E^UAS.B

(Okumura et al., 2015)

NOT suppressed by

Statement

Reference

Myo31DF^L152 has abnormal axis specification phenotype, non-suppressible by Scer\GAL4^da.PU/Myo95E^UAS.B

(Okumura et al., 2015)

Myo31DF^L152 has abnormal axis specification phenotype, non-suppressible by Scer\GAL4^da.PU/Myo95E^UAS.D

(Okumura et al., 2015)

Phenotype Manifest In

NOT Enhanced by

Statement

Reference

Myo31DF^L152 has embryonic/larval hindgut phenotype, non-enhanceable by Myo61F¹

(Okumura et al., 2015)

Myo31DF^L152 has embryonic/larval posterior midgut phenotype, non-enhanceable by Scer\GAL4^da.PU/Myo95E^UAS.B

(Okumura et al., 2015)

Myo31DF^L152 has embryonic/larval hindgut phenotype, non-enhanceable by Scer\GAL4^da.PU/Myo95E^UAS.B

(Okumura et al., 2015)

Myo31DF^L152 has embryonic/larval posterior midgut phenotype, non-enhanceable by Scer\GAL4^da.PU/Myo95E^UAS.D

(Okumura et al., 2015)

Myo31DF^L152 has embryonic/larval hindgut phenotype, non-enhanceable by Scer\GAL4^da.PU/Myo95E^UAS.D

(Okumura et al., 2015)

Myo31DF^L152 has embryonic/larval posterior midgut phenotype, non-enhanceable by Myo61F¹

(Okumura et al., 2015)

Myo31DF^L152 has embryonic/larval hindgut phenotype, non-enhanceable by Myo95E¹

(Okumura et al., 2015)

Myo31DF^L152 has embryonic/larval posterior midgut phenotype, non-enhanceable by Myo95E¹

(Okumura et al., 2015)

Myo31DF^L152 has embryonic/larval hindgut phenotype, non-enhanceable by Myo61F¹/Myo95E¹

(Okumura et al., 2015)

Myo31DF^L152 has embryonic/larval posterior midgut phenotype, non-enhanceable by Myo61F¹/Myo95E¹

(Okumura et al., 2015)

NOT suppressed by

Statement

Reference

Myo31DF^L152 has embryonic/larval posterior midgut phenotype, non-suppressible by Scer\GAL4^da.PU/Myo95E^UAS.B

(Okumura et al., 2015)

Myo31DF^L152 has embryonic/larval hindgut phenotype, non-suppressible by Scer\GAL4^da.PU/Myo95E^UAS.B

(Okumura et al., 2015)

Myo31DF^L152 has embryonic/larval posterior midgut phenotype, non-suppressible by Scer\GAL4^da.PU/Myo95E^UAS.D

(Okumura et al., 2015)

Myo31DF^L152 has embryonic/larval hindgut phenotype, non-suppressible by Scer\GAL4^da.PU/Myo95E^UAS.D

(Okumura et al., 2015)

Myo31DF^L152 has embryonic/larval posterior midgut phenotype, non-suppressible by Scer\GAL4^da.PU/Myo61F^UAS.cHa

(Okumura et al., 2015)

Myo31DF^L152 has embryonic/larval hindgut phenotype, non-suppressible by Scer\GAL4^da.PU/Myo61F^UAS.cHa

(Okumura et al., 2015)

Additional Comments

Genetic Interactions

Statement

Reference

Neither homozygous Myo95E¹ nor homozygous Myo61F¹ enhances the frequency of left/right (l/r) inversion in the posterior midgut and the hindgut seen in homozygous Myo31DF^L152 mutant embryos. As in homozygous Myo31DF^L152 mutants alone, ~80% of the double mutants exhibit the l/r reversed phenotype. No further enhancement is seen in the homozygous Myo95E¹, Myo61F¹ and Myo31DF^L152 triple mutants.

Expression of Myo95E^Scer\UAS.B under the control of Scer\GAL4^da.PU does not affect the frequency of left/right (l/r) inversion in the posterior midgut and the hindgut seen in homozygous Myo31DF^L152 mutant embryos.

Expression of Myo95E^Scer\UAS.D under the control of Scer\GAL4^da.PU does not affect the frequency of left/right (l/r) inversion in the posterior midgut and the hindgut seen in homozygous Myo31DF^L152 mutant embryos.

Expression of Myo61F^Scer\UAS.cHa under the control of Scer\GAL4^da.PU enhances the frequency of left/right (l/r) inversion in the posterior midgut and the hindgut seen in homozygous Myo31DF^L152 mutant embryos from 80% to 100%.

Expression of Myo61F^Scer\UAS.cHa under the control of Scer\GAL4^ptc-559.1 does not suppress the change in direction of male genitalia rotation seen in Myo31DF^K2/Myo31DF^L152 mutant pupae. Mutants expressing Myo61F^Scer\UAS.cHa continue to exhibit the left-handed (sinistral) rotation seen in Myo31DF^K2/Myo31DF^L152 mutations, as opposed to the dextral (right-handed) rotation seen in wild type. Expressing Myo61F^Scer\UAS.cHa in Myo31DF^K2 heterozygotes produces partial sinistral phenotypes.

Expression of Myo95E^Scer\UAS.B under the control of Scer\GAL4^ptc-559.1 does not suppress the change in direction of male genitalia rotation seen in Myo31DF^K2/Myo31DF^L152 mutant pupae. Mutants expressing Myo95E^Scer\UAS.B continue to exhibit the left-handed (sinistral) rotation seen in Myo31DF^K2/Myo31DF^L152 mutations, as opposed to the dextral (right-handed) rotation seen in wild type.

Expression of Myo31DF^{Scer\UAS.T:Avic\GFP} under the control of Scer\GAL4^ptc-559.1 completely rescues the change in direction of male genitalia rotation seen in Myo31DF^K2/Myo31DF^L152 mutant pupae. Mutants expressing Myo31DF^{Scer\UAS.T:Avic\GFP} undergo the 360[o] dextral (right-handed) rotation rather than the left-handed (sinistral) rotation seen in Myo31DF^K2/Myo31DF^L152 mutations.

(Okumura et al., 2015)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

Myo31DF^souther

(Hozumi et al., 2006)

Rescued by

Myo31DF^L152/Myo31DF^K2 is rescued by Scer\GAL4^ptc-559.1/Myo31DF^UAS.GFP

(Okumura et al., 2015)

Myo31DF^L152 is rescued by Scer\GAL4^byn-Gal4/Myo31DF^UAS.mRFP1

(Hatori et al., 2014)

Myo31DF^L152 is rescued by Scer\GAL4^Act5C.PT/Myo31DF^UAS.mRFP1

(Hatori et al., 2014)

Partially rescued by

Myo31DF^L152 is partially rescued by Myo31DF^UAS.GFP/Scer\GAL4^byn-Gal4/Scer\GAL80^ts.αTub84B

(Hozumi et al., 2008)

Comments

Expression of Myo31DF^{Scer\UAS.T:Disc\RFP-mRFP} under the control of Scer\GAL4^byn-Gal4 rescues the inverse left-right asymmetry in the hindgut positioning characteristic for Myo31DF^L152 homozygous embryos.

Induction of somatic clones of 'rescued cells', i.e. cells expressing Myo31DF^{Scer\UAS.T:Disc\RFP-mRFP} under the control of Scer\GAL4^Act5C.PT (using the Aloxg-Gal4 system) in the Myo31DF^L152 homozygote mutant background, significantly reduces the frequency of embryos with the reversed LR hindgut asymmetry as compared to non-mosaic Myo31DF^L152 mutants. The percentage of 'rescued cells' in the epithelium positively correlates with normal hindgut laterality and normal left-handed hindgut rotation occurs when about 35% of the cells in the epithelium are the 'rescued cells'. The mosaic hindgut epithelium also does not show a prominent cell-shape chirality observed either in the wild-type embryos (dextral planar cell chirality) or in the non-mosaic Myo31DF^L152 mutants (sinistral chirality) but the hindgut still undergoes a complete 90[o] left-handed rotation in majority of embryos. In the mosaic embryos, apical cell boundaries between two 'rescued cells' (R-R boundary) show on average significant dextral cell-shape chirality whereas in the 'rescued cell'- mutant cell neighbor pairs (R-M boundary) or between two mutant cells (M-M boundary) there is no significant difference between the frequency of apical cell boundaries falling in the -90[o] to 0[o] angle bin and the 90[o] to 0[o] bin. The dextral cell-shape chirality of 'rescued cells' is only evident if the cells are part of a larger clone of cells but is suppressed in smaller clones of up to 8 cells. The average length of R-R and R-M cell boundaries before and after hindgut rotation does not significantly change but the M-M boundaries are elongated after rotation.

(Hatori et al., 2014)

Expression of Myo31DF^{Scer\UAS.T:Avic\GFP} in embryos raised at 18[o]C under the control of Scer\GAL4^byn-Gal4 and Scer\GAL80^ts.αTub84B partially rescues the left-right (LR) inversion of the gut seen in Myo31DF^L152 mutants. Approximately 45% of embryos show gut inversion, compared to 40% in the absence of the driver. When embryos undergo a 60 minute temperature shift to 32[o]C at between 10 and 12.75 hours after egg laying effectively rescued the LR defects, The efficiency of rescue increasing up to 12 hours after egg laying but if the temperature shift takes place after 13 hours after egg laying rescue is less effective. The embryos shifted to 32[o]C at 12.75 hours are mostly at the late stage of germband retraction.

(Hozumi et al., 2008)

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (2)

Reported As

Symbol Synonym

Myo1D^L152

(Utsunomiya et al., 2024)

Myo31DF^L152

(Inaki et al., 2018, Okumura et al., 2015, Hatori et al., 2014, Taniguchi et al., 2011, Taniguchi et al., 2011, Hozumi et al., 2008, Taniguchi et al., 2007, Hozumi et al., 2006)

Name Synonyms

Secondary FlyBase IDs

References (9)

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