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General Information
Symbol
Dmel\Lis-1k11702
Species
D. melanogaster
Name
FlyBase ID
FBal0101591
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
lis1k11702
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

The P{lacW} insertion is in the first exon of the Lis-1 gene, 43 nucleotides downstream of the transcription start site.

Insertion components
P{lacW}Lis-1k11702
Product class / Tool use(s)
Encoded product / tool
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 ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 1 )
 

FlyBase curator comment: Interactions with Dg[086] and/or Dg[323] were detected in a Dg[086]/+ or Dg[323]/+ background which exhibits no obvious changes in muscle morphology. Nonetheless, these interactions have been captured as 'modifier' ('exacerbates') annotations here to best capture the experimental finding and the authors' intention.

Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Lis-1k11702/Lis-1G10.14 transheterozygotes show shorter and thinner giant fiber terminals and disrupted electrophysiological connection between giant fibers and TTMn (as shown by am increased latency and a severely decreased ability to follow stimuli), as compared to controls.

Lis-1E415/Lis-1k11702 results in a significant increase in the number of transported mitochondria in the wing marginal nerve in both anterograde and retrograde directions, and a small but significant increase in anterograde run velocity of mitochondria, as measured at several stages of adult life, but there is no significant difference in the total number of mitochondria, mitochondrial transport lengths or retrograde velocity, no significant difference in the proportion of motile dense-core vesicles, compared to controls.

Homozygous and hemizygous Lis-1k11702 mutant males uniformly fail to produce any progeny. The size and shape of Lis-1k11702 mutant testes appears normal, but the seminal vesicles are empty. As in wild type, Lis-1k11702 mutants produce 16 cell cysts of primary spermatocytes.

Lis-1k11702 mutant males exhibit profound defects in centrosome positioning and meiotic spindle structure. In the majority of prophase spermatocytes the centrosomes remain anchored at the cortex during G2/M rather than at the nuclear surface as is seen in wild type. The cortical centrosomes separate properly and move to opposite poles. More than 10% of Lis-1k11702 prophase spermatocytes have free centrosomes (unattached to the cortex or nuclear surface) compared to only ~3% in wild type.

Approximately 60% of prophase spermatocytes heterozygous for Lis-1k11702 have either cortical or free centrosomes. In 95% of dividing spermatocytes, meiotic spindles are typically associated with cortically positioned centrosomes compared with ~2% in wild type.

Lis-1k11702 mutant spindles are relatively long and wavy with occasional detachment of cortical spindles from spindle poles. Despite the defects in centrosome and spindle, cytokinesis and chromosome segregation appear to be grossly unaffected, as most spermatids contain a single nucleus of uniform size.

During elongation the nuclei in Lis-1k11702 mutant spermatids are round and often unattached rather than positioning themselves at the proximal tip and acquiring a needle-like shape as is seen in wild type. Basal bodies are also distributed throughout the length of elongated spermatid bundles rather localising to the proximal end. The investment cones are sparse and disorganised.

Nucleus-basal body uncoupling is seen in most Lis-1k11702/Df(2R)Jp5 mutant hemizygous spermatids. Nebenkern-basal body attachments and nucleus-nebenkern attachments are also frequently lost. Furthermore, the Nebenkern occasionally display abnormal morphology. The Nebenkern properly associates with the axoneme in early elongating Lis-1k11702 spermatids.

Only 15% of testis somatic cyst stem cells show repositioning of the mitotic spindle during anaphase in Lis-1k11702/Lis-1k13209 males compared to 72% of cases in heterozygous controls.

Eggs laid by Lis-13.1.2/Lis-1k11702 Lis-18.25.3/Lis-1k11702 Lis-1k13209/Lis-1k11702 and Lis-111.4.13/Lis-1k11702 mothers show defects in the location and morphology of the dorsal appendages. Most dorsal appendages are fused. Only about 20% of eggs laid by Lis-13.1.2/Lis-1k11702 mothers undergo cellularisation and gastrulation. Of these, about half show obvious signs of ventralisation. During early gastrulation the cephalic furrow that normally occupies a lateral position is displaced dorsally.

No obvious phenotype.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Enhanced by
Statement
Reference
Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference
Other
Statement
Reference

DCTN1-p1501, Lis-1k11702/Lis-111.4.13 has microchaeta & abdomen | ventral phenotype

DCTN1-p1501, Lis-13.3.1/Lis-1k11702 has microchaeta & abdomen | ventral phenotype

DCTN1-p1501, Lis-1k11702/Lis-17.13.1 has microchaeta & abdomen | ventral phenotype

DCTN1-p1501, Lis-18.25.3/Lis-1k11702 has microchaeta & abdomen | ventral phenotype

DCTN1-p1501, Lis-13.1.2/Lis-1k11702 has microchaeta & abdomen | ventral phenotype

DCTN1-p1501, Lis-11.2.2/Lis-1k11702 has microchaeta & abdomen | ventral phenotype

Additional Comments
Genetic Interactions
Statement
Reference

The testes of Lis-1k11702/+ ; asunf02815 mutant males are small compared to controls. There is an extreme paucity of sperm bundles and most of the cells are late G2 primary spermatocytes, indicative of a severe G2 block.

The testes of Lis-1k11702 ; asunf02815/+ males are comparable in size to controls.

Lis-1 Dys double heterozygous flies (Lis-1k11702/Df(3R)Exel6184) exhibit indirect flight muscle degeneration.

Lis-1k11702 DgO86 double heterozygous flies exhibit indirect flight muscle degeneration.

One copy of Lis-1k11702 does not enhance the indirect flight muscle degeneration seen when DysdsRNA.NH2.Scer\UAS is expressed under the control of Scer\GAL4Act.PU.

One copy of Lis-1k11702 does not enhance the indirect flight muscle degeneration seen when DgdsRNA.Scer\UAS is expressed under the control of Scer\GAL4tub.PU.

Lis-1k11702 Dg323 double heterozygous flies do not exhibit indirect flight muscle degeneration.

Eggs laid by grk6/Lis-1k11702 mothers show defects in the location and morphology of the dorsal appendages. Most dorsal appendages are fused. This is an enhancement of the grk6/+ or Lis-1k11702/+ phenotypes. Eggs laid by Egfrf24/Lis-1k11702 mothers show an enhancement of the dorsal appendage phenotype seen in Egfrf24/+ or Lis-1k11702/+ flies. The slight loss of viability phenotype seen in Lis-1k11702/Lis-13.3.1, Lis-1k11702/Lis-13.1.2, Lis-1k11702/Lis-18.25.3, Lis-1k11702/Lis-111.4.13 or Lis-1k11702/Lis-17.13.1, is enhanced by the addition of Gl1. The adult escapers from these crosses generally do not survive more than a few days. The addition of these Lis-1 transheterozygote combinations enhances the eye phenotype seen in Gl1 flies. In addition scutellar bristles of escapers flies are reduced in size and frequently lost. Most adult escapers lack bristles on the ventral side of the abdomen, and in many animals abdominal tergites are completely absent in one or more segments.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Comments

The expression of Lis-1Scer\UAS.cLa is able to rescue the Lis-1k11702/Lis-1G10.14 giant fiber anatomical defects (full rescue when driven by either Scer\GAL4shot-OK307 or Scer\GAL4GMR91H05) and electrophysiological defects (full rescue when driven by Scer\GAL4shot-OK307; partial rescue when driven by Scer\GAL4GMR91H05).

Expression of Lis-1βTub85D.T:Disc\RFP-mCherry rescues the male sterility seen in homozygous Lis-1k11702 mutants.

Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer

Separable from: l(2)k11702k11702. The lethality of the "l(2)k11702" chromosome (caused by l(2)k11702k11702) is separable from the P{lacW}Lis-1k11702 insertion.

Comments
Comments

Excision of the P{lacW} element in P{lacW}Lis-1k11702 rescues the male sterility defects seen in homozygous Lis-1k11702 mutants.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (8)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (11)