FlyBase Allele Report: Dmel\byn[5]

General Information

Symbol

Dmel\byn⁵

Species

D. melanogaster

Name

FlyBase ID

FBal0057716

Feature type

allele

Associated gene

Dmel\byn

Associated Insertion(s)

Carried in Construct

Key Links

Allele class

amorphic allele - genetic evidence

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

amorphic allele - genetic evidence

(Singer et al., 1996)

Mutagen

ethyl methanesulfonate

(Singer et al., 1996)

Progenitor genotype

Cytology

Description

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

female sterile (with byn²)

(Singer et al., 1996)

lethal (with byn¹)

(Singer et al., 1996)

lethal (with byn³)

(Singer et al., 1996)

lethal (with byn⁴)

(Singer et al., 1996)

lethal (with byn⁶)

(Singer et al., 1996)

lethal | recessive

(Singer et al., 1996)

partially lethal (with byn²)

(Singer et al., 1996)

short lived (with byn²)

(Singer et al., 1996)

Phenotype Manifest In

adult Malpighian tubule Type II cell

(Denholm et al., 2003)

circular visceral muscle fiber

(Kusch and Reuter, 1999)

egg chamber (with byn²)

(Singer et al., 1996)

embryonic/larval dorsal vessel

(Kusch and Reuter, 1999)

embryonic/larval hindgut | embryonic stage

(Kusch and Reuter, 1999)

embryonic anal pad

(Singer et al., 1996)

embryonic midgut constriction

(Singer et al., 1996)

embryonic midgut constriction 1

(Kusch and Reuter, 1999)

embryonic midgut constriction 2

(Kusch and Reuter, 1999)

embryonic midgut constriction 3

(Kusch and Reuter, 1999)

germline cell

(Kusch and Reuter, 1999)

hindgut proper primordium

(Singer et al., 1996)

longitudinal visceral muscle fiber

(Kusch and Reuter, 1999)

longitudinal visceral muscle primordium

(Kusch and Reuter, 1999)

Malpighian tubule

(Singer et al., 1996)

muscle cell of A1-7 dorsal acute muscle 1

(Kusch and Reuter, 1999)

pericardial cell

(Kusch and Reuter, 1999)

Detailed Description

Statement

Reference

Stellate cells are either absent or dramatically reduced in number in byn⁵ mutants.

(Denholm et al., 2003)

Only a few caudal visceral mesoderm cells develop. These cells form clusters that are less compact than wild type and migrate more slowly than wild type. They fail to contact the trunk mesoderm and do not distribute along the germ band. Massive apoptosis occurs in the proctodeum. Germ cell migration fails. No longitudinal visceral muscles can be detected. The circular muscle shows sporadic ruptures. No midgut constrictions are formed. The organisation of the circular visceral muscle fibre nuclei into bands is lost, and they become distributed over the gut circumference. The hindgut is severely shortened. Dorsally, the two rows of cardiac cells do not unite to form the heart vessel. Pericardial cells are missing. The dorsal acute muscle 1 is missing or fused to DA2 in many segments. These dorsal effects are underlaid by a primary defect in the number of cells in the cluster of dorsal mesoderm identified by expression of the eve marker.

(Kusch and Reuter, 1999)

Homozygous embryos exhibit greatly reduced hindgut, very short, unextended Malpighian tubules, reduced anal pads and incomplete midgut constrictions. The primary cause is ectopic cell death in the primordia. Severity of the phenotype decreases when transheterozygous with other byn alleles. Transheterozygotes with byn² allow some (1-25%) survive to adulthood, no escapers are obtained from transheterozygotes with byn¹, byn³, byn⁴ and byn⁶. Escaper adults appear morphologically normal but females are sterile (no eggs in the egg chambers have progressed beyond stage 7 of ovarian development). Escapers usually die 1-2 days after eclosion.

(Singer et al., 1996)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Phenotype Manifest In

Suppressor of

Statement

Reference

byn⁵ is a suppressor of embryonic/first instar larval cuticle | maternal effect phenotype of tor^12D

(Li and Li, 2003)

Other

Statement

Reference

byn⁵, fkh⁶ has longitudinal visceral muscle primordium phenotype

(Kusch and Reuter, 1999)

Additional Comments

Genetic Interactions

Statement

Reference

In byn⁵, fkh⁶ double mutants, no caudal visceral mesoderm cells develop at all.

(Kusch and Reuter, 1999)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Partially complements

byn²

(Singer et al., 1996)

Fails to complement

byn¹

(Singer et al., 1996)

byn³

(Singer et al., 1996)

byn⁴

(Singer et al., 1996)

byn⁶

(Singer et al., 1996)

Partially rescued by

byn⁵ is partially rescued by Scer\GAL4^447.2/byn^UAS.cKa

(Kusch and Reuter, 1999)

Comments

The caudal visceral mesoderm phenotype of byn⁵ is rescued by byn^Scer\UAS.cKa, Scer\GAL4^447.2, though the hindgut of rescued animals remains rudimentary. Germ cell migration defect is almost completely rescued, as are dorsal mesodermal structures.

(Kusch and Reuter, 1999)

P{Trg20} can rescue the lethality of byn⁵/Df(3L)vin4 transheterozygous embryos.

(Singer et al., 1996)

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

26186

byn⁵ e^*/TM6B, Tb¹ ca¹

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (1)

Reported As

Symbol Synonym

byn⁵

(Ismat et al., 2010)

Name Synonyms

Secondary FlyBase IDs

References (8)

Report Sections

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