FlyBase Allele Report: Dmel\mei-P26[1]

General Information

Symbol

Dmel\mei-P26¹

Species

D. melanogaster

Name

FlyBase ID

FBal0095291

Feature type

allele

Associated gene

Dmel\mei-P26

Associated Insertion(s)

P{lacW}mei-P26-1

Carried in Construct

Key Links

Allele class

hypomorphic allele - genetic evidence

Mutagen

Delta2-3 transposase

Nature of the Allele

Allele class

hypomorphic allele - genetic evidence

(Page et al., 2000, Page et al., 1999, Sekelsky et al., 1999)

Mutagen

Delta2-3 transposase

(Sekelsky et al., 1999)

Progenitor genotype

Associated Insertion(s)

P{lacW}mei-P26-1

Cytology

Description

P{lacW} insertion within the first intron.

(Page et al., 2000)

Allele components

Component

Use(s)

Inserted element

P{lacW}

enhancer trap

Encoded product / tool

lacZ

reporter enzyme

Tagged with

Tag:NLS(P)

nuclear protein localization tag

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 meiotic cell cycle

(Page et al., 1999)

abnormal meiotic cell cycle | semidominant

(Sekelsky et al., 1999)

female semi-fertile

(Page et al., 1999)

male fertile

(Page et al., 2000)

Phenotype Manifest In

egg chamber (with mei-P26^fs1)

(Liu et al., 2009)

nurse cell

(Page et al., 2000)

nurse cell (with mei-P26^fs1)

(Liu et al., 2009)

testis

(Page et al., 2000)

Detailed Description

Statement

Reference

mei-P26¹/mei-P26^fs1 ovaries are mostly wild-type in appearance, with less than 5% of egg chambers having fewer or more than 15 nurse cells or being incorrectly patterned.

(Liu et al., 2009)

Homozygous females show 17.3% X chromosome nondisjunction and 8.4% 4th chromosome nondisjunction. mei-P26¹/mei-P26^fs1 females show 22.4% X chromosome nondisjunction and 18.1% 4th chromosome nondisjunction. The majority of aberrant X chromosome segregation in mutant females appears to be due to nondisjunction rather than chromosome loss. The X chromosome nondisjunction appears to be due the failed segregation of nonexchange tetrads. Recombination is strongly decreased in the distal part of the 2L chromosome arm in homozygous females, but higher frequencies of recombination than wild type are seen in the proximal region of the chromosome arm, near the centric heterochromatin. Recombination frequency on chromosome 2 is decreased in mei-P26¹/mei-P26^fs1 females and the recombination distribution is polar. Homozygous ovaries rarely have tumourous egg chambers (0.7%). Defects in nurse cell number are seen, with egg chambers often having too many or too few nurse cells. Hemizygous males produce motile spermatozoa and are fertile. Highly refractile degenerating cysts are seen in the testes.

(Page et al., 2000)

Females homozygous for mei-P26¹ display a 70-90% reduction in meiotic recombination and high levels of nondisjunction. Although mei-P26¹ homozygotes also show a reduction in fertility, combinations with deficiencies for the region result in almost complete sterility, suggesting that mei-P26¹ is a hypomorph.

(Page et al., 1999)

Mutant for female meiotic segregation: 18.3% X chromosome exceptions from X/X females. 14.3% 4th chromosome exceptions from X/X females. Recombination defective mutant. Homozygous females show meiotic recombination reduced by 70-90%. Heterozygosity for mei-P26¹ or a deficiency for mei-P26 reduces exchange by one third.

(Sekelsky et al., 1999)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Other

Statement

Reference

bam^Δ86, mei-P26¹ has male sterile phenotype

(Page et al., 2000)

bam[+]/bam^Δ86, mei-P26¹ has female semi-sterile phenotype

(Page et al., 2000)

Phenotype Manifest In

Enhanced by

Statement

Reference

mei-P26^fs1/mei-P26¹ has oocyte phenotype, enhanceable by vas^PH165/vas¹

(Liu et al., 2009)

mei-P26^fs1/mei-P26¹ has egg chamber phenotype, enhanceable by vas^PH165/vas¹

(Liu et al., 2009)

mei-P26^fs1/mei-P26¹ has nurse cell phenotype, enhanceable by vas^PH165/vas¹

(Liu et al., 2009)

mei-P26¹ has ovary phenotype, enhanceable by bam[+]/bam^Δ86

(Page et al., 2000)

Other

Statement

Reference

bam^Δ86, mei-P26¹ has spermatid phenotype

(Page et al., 2000)

bam^Δ86, mei-P26¹ has egg chamber phenotype

(Page et al., 2000)

bam[+]/bam^Δ86, mei-P26¹ has egg chamber phenotype

(Page et al., 2000)

Additional Comments

Genetic Interactions

Statement

Reference

More than 50% of vas¹/vas^PH165 ; mei-P26¹/mei-P26^fs1 egg chambers are tumorous and fail to differentiate nurse cells and oocytes. The double mutant egg chambers contain mostly early-stage cystocytes as they contain either punctate spectrosomes or branched fusomes.

(Liu et al., 2009)

mei-P26¹/Y ; bam^Δ86/+ males are completely sterile. Spermatid differentiation fails to progress in these males. mei-P26¹/mei-P26¹ ; bam^Δ86/+ females show a severe decrease in fertility compared to mei-P26¹/mei-P26¹ females, due to an increase in the formation of ovarian tumours and other egg chamber defects. Recombination is also severely decreased in these females. mei-P26¹/+ ; bam^Δ86/+ females have normal fertility.