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General Information
Symbol
Dmel\egl1
Species
D. melanogaster
Name
FlyBase ID
FBal0003574
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
eglWU50
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Comment:

An unspecified mutation in the splice acceptor site. The splice site mutation has been arbitrarily mapped by a FlyBase curator to the first base of the splice acceptor site.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Amino acid replacement: A399T. Also a splice site mutation between amino acids 787 and 788, causing a frame shift after residue 777.

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
Phenotype Manifest In
Detailed Description
Statement
Reference

Ovarian cysts from egl1/egl2 animals do not accumulate autolysosomes.

egl1 mutant terminal cells are indistinguishable from wild type.

egl1/egl4 third instar larvae have no defects in the localisation of nuclei in the optic stalk or retina.

Embryos derived from egl3e/egl1 mothers mated to egl4/+ fathers often show a disrupted epidermis. At stage 13, the salivary gland placode area is often disrupted. Salivary gland morphogenesis is disrupted in that cells of the placode often do not change their apices in a coordinated way; the invagination hole appears too large and extended; and the invaginated portion of the glands often has an irregular shape.

Meiosis is initiated in all cells in region 2a of the egl1/egl2 germarium, in contrast to the normal initiation of meiosis in two to four cells.

12% of neuroblast mitoses are more than 45o off-axis in embryos derived from egl3e/egl1 females (in contrast to wild type where all neuroblast divisions are oriented within 45o of the apicobasal axis). The average length of metaphase spindles in these mutant neuroblasts is significantly less than normal.

In egl1 mutant ovaries, all 16-cyst cells enter the meiotic cycle and form synaptonemal complexes. However, this meiotic state is not stably maintained and ultimately all 16 cystocytes exit the meiotic cycle and enter the endocycle.

All 16 cells of developing egl1/egl4 mutant ovaries initially enter mitosis and form a synaptonemal complex. The synaptonemal complex dissolves in later egg chambers and all 16 cells become polyploid nurse cells.

Mitochondria behave normally in dividing cysts in mutant females. However, in 16-cell cysts, most of the mitochondria in each cystocyte aggregate on the fusome remnants at the ring canals. These mitochondrial aggregates are retained and grow in size during subsequent follicle development.

The centrosomes of egl1/egl2 mutant cysts migrate along the fusome and accumulate in a single cell in late region-2b and region-3 cysts (as occurs in wild type) but they do not move to the posterior of this cell and remain associated with the remnants of the fusome (in contrast to wild type). The cell that accumulates the centrosomes contains the largest portion of the degenerating fusome. egl1/Df(2R)bw-S46 cysts do not show a visible MTOC in regions 2 or 3 and microtubules are uniformly distributed in all cells of the cyst, in contrast to wild type.

Oocytes are not determined in mutant ovaries and all 16 cells of the germ-line cyst eventually take on a nurse cell fate.

The synaptonemal complex (SC) forms with equal intensity in all 16 cells of the germline cyst in early region 2a in egl2/egl1 females. All of the cells appear to be fully synapsed, but the SC looks somewhat thinner than in wild type. The SC is not maintained, however, and disappears before the cysts reach region 2b. The 16 cells form nurse cells.

Homozygous egg chambers contain 16 nurse cells but no oocyte.

Cysts do not form an oocyte in homozygous females. As in wild-type, cysts flatten to extend across the width of the germarium in region 2b and then round up to form a sphere as they move into region 3. However, none of the germ cells protrude into the follicle cell layer in region 3.

Fusomes in the cysts of egl1/egl2 ovaries appear to form normally.

All 16 cells of the cyst become polyploid nurse cells, none of the cystoblast daughters develops as an oocyte. Development of the 16-cell cluster ceases at about stage 6 of oogenesis, no cell accumulates yolk and eventually the cluster degenerates. Transplantation of wild type pole cells into mutant flies allows normal oocyte development, transplantation of mutant pole cells into wild type flies causes a block in oocyte determination.

16 cell vitellarial cysts cease to enlarge partway down the vitellarium and are eventually phagocytosed. Cyst production dynamics are normal. All 16 nuclei in a cyst enter meiosis; the chromatin condenses and synaptonemal complex is present. Later all 16 lose the synaptonemal complex and assume nurse cell characteristics. Cell shape changes within the cyst are normal as the cysts pass down the germarium. Synaptonemal complex is of normal width and is apparently normal in substructure, but throughout pachytene it maintains the extreme thinness typical of wild-type synaptonemal complex during zygotene. Most "pachytene" nuclei in egl mutant cysts have zygotene numbers of synaptonemal complex segments as well as zygotene thinness. The nuclei do mount both early and late recombination nodules, at normal positions within the germarium. Number of recombination nodules per nucleus is comparable to that in wild type pro-oocyte. The onset of cytoplasmic flow is delayed. In mid-vitellarium the 16 cells remain the same size. Ring canals frequently do not enlarge as much as they should, and are more likely to be lacking their inner lining than in wild type. The fusome is apparently normal. Centrioles and mitochondria orient normally. Centriole replication continues. Mitochondria indicate that the ring canals may be unusually difficult to pass through.

Oogenesis is blocked at an early stage, oocyte fails to differentiate properly and all 16 cells develop as nurse cells.

In germaria of egl1/egl2 females the microtubule organizing center that forms is unstable.

Double mutants with otu5 mutants display degenerate egg chambers, mutant phenotypes are cumulative.

16 nurse cells in a follicle rather than 15 and an oocyte. Follicle breaks down after stage 7. Normal morphological markers for polarity, such as gradient in size of nurse cell nuclei, can be identified in mutant follicles, but their spatial organisation is disturbed. Up to stage 5 the relative position of the presumptive ooocyte is normal, after stage 5 it is often found in aberrant positions: mis-positioning is correlated with aberrant pattern of extracellular ionic currents. Mutant follicles have differentiating follicular epithelium in patches, whereas wild type only has such cells around the oocyte.

Oocyte determination is blocked, egg chambers fail to differentiate an oocyte.

Abdominal defect: no eggs.

Egg chambers contain 16 nurse cells and no oocyte.

female-sterile. anterior germarium. In contrast to wild-type, in all egl alleles all sixteen cells per cyst enter pachytene; subsequently all sixteen revert to nurse-cell morphology and behavior (Carpenter). Egg chambers increase in volume along the ovariole, but do not take up yolk. No chorion is formed. BicD/+ females simultaneously heterozygous for egl1 or egl2 fail to form double-abdomen embryos (Mohler and Wieschaus, 1986). Defect in cell fate detectable in

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Suppressed by
Statement
Reference

egl3e/egl1 has embryonic neuroblast & spindle phenotype, suppressible by inschs.PKb

Enhancer of
NOT Enhancer of
Statement
Reference
NOT Suppressor of
Statement
Reference
Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

The frequency of cuticular segmentation phenotypes in eve1.27/+ first instar larvae is significantly enhanced in animals with a egl3e/egl1 mutant mother. The frequency of cuticular segmentation phenotypes in ftz13/+ first instar larvae is significantly enhanced in animals with a egl3e/egl1 mutant mother. The frequency of cuticular segmentation phenotypes in hi22/+ first instar larvae is significantly enhanced in animals with a egl3e/egl1 mutant mother. The frequency of cuticular segmentation phenotypes in Kr1/+ first instar larvae is not significantly changed in animals with a egl3e/egl1 mutant mothers, however the identity of segments affected differs slightly: there are less defects in A1 and A2, and more defects in A3. The frequency of cuticular segmentation phenotypes in wgl-17/+ first instar larvae is not significantly changed in animals with a egl3e/egl1 mutant mother.

Expression of inschs.PKb rescues the average length of metaphase spindles in neuroblasts of embryos derived from egl3e/egl1 females to a value similar to wild type.

mio2; egl1 double homozygotes have a phenotype significantly stronger than either single mutant: All cystoblasts lack obvious synaptonemal complexes.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
Comments
Comments

When transheterozygous with a deficiency, ovary size is no smaller than for the egl1 homozygote.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (40)