FlyBase Allele Report: Dmel\Lis-1[k11702]

General Information

Symbol

Dmel\Lis-1^k11702

Species

D. melanogaster

Name

FlyBase ID

FBal0101591

Feature type

allele

Associated gene

Dmel\Lis-1

Associated Insertion(s)

P{lacW}Lis-1^k11702

Carried in Construct

Also Known As

lis1^k11702

Key Links

Genomic Maps

JBrowse

Allele class

Mutagen

P-element activity

Nature of the Allele

Allele class

Mutagen

P-element activity

(Lei and Warrior, 2000, Spradling, 1999.12.9, Spradling et al., 1999)

Progenitor genotype

Associated Insertion(s)

P{lacW}Lis-1^k11702

Cytology

Description

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

(Lei and Warrior, 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

transposable_element_insertion_site

2R:16,178,854..16,178,854 [+]

(Sitaram et al., 2012, Lei and Warrior, 2000, Spradling, 1999.12.9, Spradling et al., 1999)

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 ( 1 )

Disease

Interaction

References

exacerbates muscular dystrophy

modeled by Dg^O86

(Kucherenko et al., 2011)

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.

(Kucherenko et al., 2011)

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal neuroanatomy | adult stage (with Lis-1^G10.14)

(Kudumala et al., 2017)

abnormal neurophysiology | adult stage (with Lis-1^G10.14)

(Kudumala et al., 2017)

abnormal size | adult stage (with Lis-1^G10.14)

(Kudumala et al., 2017)

lethal | recessive

(Lei and Warrior, 2000)

male sterile

(Sitaram et al., 2012)

sterile (with Lis-1^1.2.2)

(Lei and Warrior, 2000)

sterile (with Lis-1^3.1.2)

(Lei and Warrior, 2000)

sterile (with Lis-1^8.25.3)

(Lei and Warrior, 2000)

sterile (with Lis-1^11.4.13)

(Lei and Warrior, 2000)

Phenotype Manifest In

axon | adult stage (with Lis-1^E415)

(Vagnoni et al., 2016)

centrosome

(Sitaram et al., 2012)

cyst progenitor cell (with Lis-1^k13209)

(Cheng et al., 2011)

dorsal appendage (with Lis-1^1.2.2)

(Lei and Warrior, 2000)

dorsal appendage (with Lis-1^3.1.2)

(Lei and Warrior, 2000)

dorsal appendage (with Lis-1^8.25.3)

(Lei and Warrior, 2000)

dorsal appendage (with Lis-1^11.4.13)

(Lei and Warrior, 2000)

dorsal appendage (with Lis-1^k13209)

(Lei and Warrior, 2000)

giant fiber neuron | adult stage (with Lis-1^G10.14)

(Kudumala et al., 2017)

investment cone

(Sitaram et al., 2012)

marginal nerve | adult stage (with Lis-1^E415)

(Vagnoni et al., 2016)

mitochondrion | adult stage (with Lis-1^E415)

(Vagnoni et al., 2016)

Nebenkern (with Df(2R)Jp5)

(Sitaram et al., 2012)

spermatid

(Sitaram et al., 2012)

spermatid (with Df(2R)Jp5)

(Sitaram et al., 2012)

spermatocyte

(Sitaram et al., 2012)

spindle

(Sitaram et al., 2012)

spindle (with Lis-1^k13209)

(Cheng et al., 2011)

Detailed Description

Statement

Reference

Lis-1^k11702/Lis-1^G10.14 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.

(Kudumala et al., 2017)

Lis-1^E415/Lis-1^k11702 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.

(Vagnoni et al., 2016)

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

Lis-1^k11702 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-1^k11702 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-1^k11702 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-1^k11702 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-1^k11702 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-1^k11702/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-1^k11702 spermatids.

(Sitaram et al., 2012)

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

(Cheng et al., 2011)

Eggs laid by Lis-1^3.1.2/Lis-1^k11702 Lis-1^8.25.3/Lis-1^k11702 Lis-1^k13209/Lis-1^k11702 and Lis-1^11.4.13/Lis-1^k11702 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-1^3.1.2/Lis-1^k11702 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.

(Lei and Warrior, 2000)

No obvious phenotype.

(Spradling et al., 1999)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

Lis-1^k11702/Lis-1^11.4.13 has partially lethal - majority die phenotype, enhanceable by DCTN1-p150^Gl-1

(Lei and Warrior, 2000)

Lis-1^1.2.2/Lis-1^k11702 has partially lethal - majority die phenotype, enhanceable by DCTN1-p150^Gl-1

(Lei and Warrior, 2000)

Lis-1^3.3.1/Lis-1^k11702 has partially lethal - majority die phenotype, enhanceable by DCTN1-p150^Gl-1

(Lei and Warrior, 2000)

Lis-1^k11702/Lis-1^7.13.1 has partially lethal - majority die phenotype, enhanceable by DCTN1-p150^Gl-1

(Lei and Warrior, 2000)

Lis-1^8.25.3/Lis-1^k11702 has partially lethal - majority die phenotype, enhanceable by DCTN1-p150^Gl-1

(Lei and Warrior, 2000)

Lis-1^3.1.2/Lis-1^k11702 has partially lethal - majority die phenotype, enhanceable by DCTN1-p150^Gl-1

(Lei and Warrior, 2000)

Other

Statement

Reference

Lis-1[+]/Lis-1^k11702, asun^f02815 has abnormal meiotic cell cycle phenotype

(Sitaram et al., 2012)

Lis-1^k11702, cni^AA12 has wild-type phenotype

(Lei and Warrior, 2000)

Phenotype Manifest In

Enhanced by

Statement

Reference

Lis-1^k11702 has dorsal appendage phenotype, enhanceable by Egfr^f24

(Lei and Warrior, 2000)

Lis-1^k11702 has dorsal appendage phenotype, enhanceable by grk⁶

(Lei and Warrior, 2000)

Enhancer of

Statement

Reference

Lis-1^k11702/Lis-1^11.4.13 is an enhancer of eye phenotype of DCTN1-p150^Gl-1

(Lei and Warrior, 2000)

Lis-1^3.1.2/Lis-1^k11702 is an enhancer of eye phenotype of DCTN1-p150^Gl-1

(Lei and Warrior, 2000)

Lis-1^k11702 is an enhancer of dorsal appendage phenotype of grk³

(Lei and Warrior, 2000)

Lis-1^3.3.1/Lis-1^k11702 is an enhancer of eye phenotype of DCTN1-p150^Gl-1

(Lei and Warrior, 2000)

Lis-1^k11702/Lis-1^7.13.1 is an enhancer of eye phenotype of DCTN1-p150^Gl-1

(Lei and Warrior, 2000)

Lis-1^8.25.3/Lis-1^k11702 is an enhancer of eye phenotype of DCTN1-p150^Gl-1

(Lei and Warrior, 2000)

NOT Enhancer of

Statement

Reference

Lis-1[+]/Lis-1^k11702 is a non-enhancer of indirect flight muscle cell phenotype of Dys^RNAi.NH2.UAS, Scer\GAL4^Act.PU

(Kucherenko et al., 2011)

Lis-1[+]/Lis-1^k11702 is a non-enhancer of indirect flight muscle cell phenotype of Dg^RNAi.UAS, Scer\GAL4^Act.PU

(Kucherenko et al., 2011)

Other

Statement

Reference

Lis-1[+]/Lis-1^k11702, asun^f02815 has testis phenotype

(Sitaram et al., 2012)

Df(3R)Exel6184/+, Lis-1^k11702 has indirect flight muscle cell phenotype

(Kucherenko et al., 2011)

Dg[+]/Dg^O86, Lis-1^k11702 has indirect flight muscle cell phenotype

(Kucherenko et al., 2011)

DCTN1-p150^Gl-1, Lis-1^k11702/Lis-1^11.4.13 has macrochaeta phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^k11702/Lis-1^11.4.13 has abdominal tergite phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^k11702/Lis-1^7.13.1 has abdominal tergite phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^k11702/Lis-1^7.13.1 has microchaeta & abdomen | ventral phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^8.25.3/Lis-1^k11702 has macrochaeta phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^8.25.3/Lis-1^k11702 has abdominal tergite phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^8.25.3/Lis-1^k11702 has microchaeta & abdomen | ventral phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^3.1.2/Lis-1^k11702 has macrochaeta phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^3.1.2/Lis-1^k11702 has abdominal tergite phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^3.1.2/Lis-1^k11702 has microchaeta & abdomen | ventral phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^k11702/Lis-1^11.4.13 has microchaeta & abdomen | ventral phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^1.2.2/Lis-1^k11702 has macrochaeta phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^1.2.2/Lis-1^k11702 has abdominal tergite phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^1.2.2/Lis-1^k11702 has microchaeta & abdomen | ventral phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^3.3.1/Lis-1^k11702 has macrochaeta phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^3.3.1/Lis-1^k11702 has abdominal tergite phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^3.3.1/Lis-1^k11702 has microchaeta & abdomen | ventral phenotype

(Lei and Warrior, 2000)

DCTN1-p150^Gl-1, Lis-1^k11702/Lis-1^7.13.1 has macrochaeta phenotype

(Lei and Warrior, 2000)

Additional Comments

Genetic Interactions

Statement

Reference

The testes of Lis-1^k11702/+ ; asun^f02815 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-1^k11702 ; asun^f02815/+ males are comparable in size to controls.

(Sitaram et al., 2012)

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

Lis-1^k11702 Dg^O86 double heterozygous flies exhibit indirect flight muscle degeneration.

One copy of Lis-1^k11702 does not enhance the indirect flight muscle degeneration seen when Dys^{dsRNA.NH2.Scer\UAS} is expressed under the control of Scer\GAL4^Act.PU.

One copy of Lis-1^k11702 does not enhance the indirect flight muscle degeneration seen when Dg^{dsRNA.Scer\UAS} is expressed under the control of Scer\GAL4^tub.PU.

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

(Kucherenko et al., 2011)

Eggs laid by grk⁶/Lis-1^k11702 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-1^k11702/+ phenotypes. Eggs laid by Egfr^f24/Lis-1^k11702 mothers show an enhancement of the dorsal appendage phenotype seen in Egfr^f24/+ or Lis-1^k11702/+ flies. The slight loss of viability phenotype seen in Lis-1^k11702/Lis-1^3.3.1, Lis-1^k11702/Lis-1^3.1.2, Lis-1^k11702/Lis-1^8.25.3, Lis-1^k11702/Lis-1^11.4.13 or Lis-1^k11702/Lis-1^7.13.1, 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.

(Lei and Warrior, 2000)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

Lis-1^k11702/Lis-1^G10.14 is rescued by Lis-1^UAS.cLa/Scer\GAL4^shot-OK307

(Kudumala et al., 2017)

Lis-1^k11702 is rescued by Lis-1^{βTub85D.mCherry}

(Sitaram et al., 2012)

Partially rescued by

Lis-1^k11702/Lis-1^G10.14 is partially rescued by Scer\GAL4^GMR91H05/Lis-1^UAS.cLa

(Kudumala et al., 2017)

Comments

The expression of Lis-1^Scer\UAS.cLa is able to rescue the Lis-1^k11702/Lis-1^G10.14 giant fiber anatomical defects (full rescue when driven by either Scer\GAL4^shot-OK307 or Scer\GAL4^GMR91H05) and electrophysiological defects (full rescue when driven by Scer\GAL4^shot-OK307; partial rescue when driven by Scer\GAL4^GMR91H05).

(Kudumala et al., 2017)

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

(Sitaram et al., 2012)

Images (0)

Mutant

Wild-type

Stocks (2)

Bloomington

10179

y¹ w^67c23; P{lacW}Lis-1^k11702/CyO

Kyoto

111018

y^d2 w¹¹¹⁸ P{ey-FLP.N}2 P{5xglBS-lacZ.38-1}TPN1; P{neoFRT}42D P{lacW}Lis-1^k11702 /CyO y⁺

Notes on Origin

Discoverer

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

(Spradling, 1999.12.9)

Comments

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

(Sitaram et al., 2012)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (8)

Reported As

Symbol Synonym

DLis¹¹⁷⁰²

(Lei and Warrior, 2000)

Lis-1^k11702

(Sitaram et al., 2012)

Lis1^k11702

(Vagnoni et al., 2016, Marrone et al., 2011)

Paf-AHβ^k11702

lis-1^k11702

(Kucherenko et al., 2011)

lis1^K11702

(Schulman et al., 2014)

lis1^k11702

(Kudumala et al., 2017, Dix et al., 2013, Cheng et al., 2011)

n(2)k11702

(Spradling, 1999.12.9, Spradling et al., 1999)

Name Synonyms

Secondary FlyBase IDs

References (11)

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