FB2024_03 , released June 25, 2024
Allele: Dmel\spn-D2
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General Information
Symbol
Dmel\spn-D2
Species
D. melanogaster
Name
FlyBase ID
FBal0016040
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
spn-D349, spnD349
Key Links
Nature of the Allele
Progenitor genotype
Cytology
Description
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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

Homozygous females show a high frequency (more than 50%) of region 3 cysts with two pro-oocytes (as assayed by c(3)G staining) compared to a frequency of only 9.5% in wild type.

In spn-D2 oocytes, both the anterior and later posterior microtubule-organizing centers are much less prominent than in wild-type oocytes.

Over half of spn-D2 eggs show a fused dorsal appendage phenotype and 11% of eggs have no dorsal appendages at all.

spn-D2/spn-D1 larvae are not sensitive to MMS.

spn-D2/spn-D2 females exhibit low fertility, and meioses show reduced frequency of crossing over along most of chromosome 2, but not in the centromeric regions, as compared to wild type.

spn-D2/spn-D1 females exhibit low fertility, and meioses show reduced frequency of crossing over along most of chromosome 2, as compared to wild type.

43% of eggs derived from homozygous females have wild-type eggshells, 57% have mutant eggshells, with 21% having dorsalised eggs with dorsal appendage material around the lateral and ventral side of the egg. 70% of eggs derived from spn-D1/spn-D2 females have mutant eggshells and defects in karyosome morphology are seen in the mutant egg chambers.

In contrast to wild-type ovaries, where the synaptonemal complex (SC) is always restricted to the oocyte by region 2b, spn-D2 mutant females show a significant delay in the process, with cysts with more than 1 cell in synapsis in region 3 of the germarium and one cell in synapsis in stage 2 of the vitellarium.

Hemizygotes are viable. spn-D1/spn-D2 larvae show normal sensitivity to methyl methanesulfonate. Recombination frequency is 10-25% of normal levels in homozygous females, and X chromosome non-disjunction is increased 100-fold compared to wild-type.

Hemizygous eggs exhibit either a strong or weak ventralised phenotype: eggs are longer than wild type and are completely symmetric along the DV axis or the eggs display fused dorsal appendages. Egg chambers of females exhibit a partially penetrant disruption in the positioning of the oocyte which can be located anywhere in the egg chamber. Germline clones in egg chambers are composed of wild type follicle cells, mutant nurse cells, misplaced oocyte, oocytes that give rise to ventralised eggs and oocytes that lack a karyosome.

strong

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

spn-D2 has phenotype, enhanceable by spn-A3

spn-D2 has oocyte phenotype, enhanceable by spn-A3

spn-D2 has oocyte phenotype, enhanceable by spn-B1

spn-D2 has oocyte phenotype, enhanceable by spn-E1

Suppressed by
Statement
Reference

spn-D2 has microtubule organizing center & oocyte phenotype, suppressible by lokp6/lokp6

spn-D2/spn-D1 has karyosome phenotype, suppressible by mei-41D3

spn-D2/spn-D1 has karyosome phenotype, suppressible | partially by mei-41D1

Enhancer of
Statement
Reference

spn-D2 is an enhancer of phenotype of spn-A3

spn-D2 is an enhancer of oocyte phenotype of spn-B1

spn-D2 is an enhancer of oocyte phenotype of spn-E1

Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

The microtubule-organizing center phenotype of spn-D2 oocytes is suppressed by the lokp6 mutation.

The fused dorsal appendage phenotype of spn-D2 eggs is suppressed by lokp6.

The eggshell defects seen in eggs derived from spn-D1/spn-D2 females are completely suppressed if the females are also homozygous for mei-W68unspecified. The karyosome defects seen in spn-D1/spn-D2 egg chambers are also suppressed by mei-W68unspecified. The eggshell defects seen in eggs derived from spn-D1/spn-D2 females are suppressed if the females also carry mei-41unspecified. The karyosome defects seen in spn-D1/spn-D2 egg chambers are only slightly suppressed by mei-41D1 but are strongly suppressed by mei-41D3.

The phenotype of a delay in the restriction of the synaptonemal complex seen in the female germline of spn-D2 or spn-A3 single mutants is enhanced in spn-D2 spn-A1 double mutants.

Has no effect on the frequency of X-Y chromosome nondisjunction seen in Df(1)X-1-53B males.

Double mutants with spn-A3, spn-B1 or spn-E1 increases the oocyte mispositioning frequency. Almost all oocytes lack a karyosome and the oocyte chromosomes are arranged instead in thread-like figures with irregular shape. Double mutant mothers with fs(1)K101 lay dorsalised eggs, the dorsal appendages form a collar around the entire circumference of the egg. This phenotype is indistinguishable from that of fs(1)K101 single mutants.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Fails to complement
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (13)