FB2024_03 , released June 25, 2024
Allele: Dmel\mei-41RT1
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General Information
Symbol
Dmel\mei-41RT1
Species
D. melanogaster
Name
FlyBase ID
FBal0046106
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Allele class
Nature of the Allele
Allele class
Progenitor genotype
Associated Insertion(s)
Cytology
Description

Insertion of P-element into the same SalI-EcoRI genomic fragment that includes the insertion in mei-41RT2, though in opposite orientation to P-element in mei-41RT2.

Insertion of a P-element.

Mutations Mapped to the Genome
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 eye discs show severe defects in hydroxyurea-induced G2 arrest, with the number of mitotic cells remaining high after treatment, in contrast to wild type.

X-ray irradiation of wild-type third-instar wing imaginal discs induces cell cycle arrest within 1 hour. In contrast, X-ray irradiation of mei-41RT1 mutant larvae fails to induce cell cycle arrest.

Mutant larvae fail to undergo G2 arrest in response to ionizing radiation, in contrast to wild type (assayed by scoring mitotic cells in larval eye-antennal imaginal discs).

Mutant larvae fail to undergo intra-S phase arrest in response to ionizing radiation, in contrast to wild type (assayed by scoring mitotic cells in larval brains).

Mutants are hypersensitive to irradiation, showing only 3.3% eclosion after exposure to 10 Gray (90.2% of wild-type larvae eclose at this dose).

Mutant larvae lack the normal checkpoint response (a steep decline in the number of G2 cells entering mitosis) when irradiated with either 500 or 4000 rad of X rays.

Mutant wing discs do not show cell cycle block after X-ray irradiation (in contrast to wild type), with the number of mitotic cells in mutant irradiated wing discs being similar to the number of mitotic cells in untreated mutant wing discs.

The number of mitotic cells in the mei-41RT1 eye disc is unchanged following irradiation, in contrast to wild-type discs where very few cells are in M phase after irradiation. The morphology of the eye disc and adult eye is normal in unirradiated mei-41RT1 animals.

Homozygotes are sensitive to MMS and show female sterility.

Methyl methanesulfonate sensitive, exposure causes lethality. Frequency of XO males and XXY females suggests high rates of chromosome loss.

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

mei-41D5/mei-41RT1 has lethal | embryonic stage phenotype, enhanceable by MCPH1Z1861/MCPH1[+]

Suppressed by
Statement
Reference
Enhancer of
NOT Enhancer of
Statement
Reference
Suppressor of
NOT Suppressor of
Statement
Reference

mei-41RT1 is a non-suppressor of visible phenotype of Fcp1c.UAS, Scer\GAL4en-e16E

mei-41RT1 is a non-suppressor of lethal phenotype of Fcp1c.UAS, Scer\GAL4da.G32

Other
Phenotype Manifest In
Enhancer of
Statement
Reference

mei-41RT1 is an enhancer of chromosome & neuroblast | third instar larval stage 2 phenotype of tefuunspecified

mei-41RT1 is an enhancer of chromosome & neuroblast | third instar larval stage 2 phenotype of nbs1

NOT Enhancer of
Statement
Reference

mei-41RT1 is a non-enhancer of wing phenotype of Fcp1c.UAS, Scer\GAL4en-e16E

Suppressor of
NOT Suppressor of
Statement
Reference

mei-41RT1 is a non-suppressor of wing phenotype of Fcp1c.UAS, Scer\GAL4en-e16E

Additional Comments
Genetic Interactions
Statement
Reference

The ventralised eggshell phenotype seen in eggs derived from homozygous CycGHR7 females is suppressed in more than 90% of eggs if the females are also carrying mei-41RT1/Df(1)BSC772.

Df(3R)d58/Df(3R)d189, P{CaSpeR-DTLum} (i.e. moi mutants) die at later phases or even hatch when they are also mutant for mei-41RT1.

P{lacW}moiS096713/Df(3R)d189, P{CaSpeR-DTLum} (i.e. moi mutant) neuroblasts show fewer anaphase chromosome bridges when mei-41RT1 is present.

Df(3R)d58/Df(3R)d189, P{CaSpeR-DTLum} (i.e. moi mutant) neuroblasts show fewer anaphase chromosome bridges when mei-41RT1 is present.

MCPH1Z1861 dominantly enhances the embryonic lethality caused by mei-41RT1/mei-41D5.

The number of mitotic cells is slightly but significantly higher in hydroxyurea-treated discs from mei-41RT1/nej3 transheterozygotes compared with heterozygous mei-41RT1 controls.

Expression of nej+t16 suppresses the mitosis phenotypes in response to hydroxyurea seen in mei-41RT1/nej3 transheterozygotes.

mei-41RT1 ; tefustg double mutant larvae show complete loss of the checkpoint response when irradiated with either 500 or 4000 rad of X rays.

The chromosome fusion phenotype seen in third instar larval neuroblasts of tefuunspecified mutants is enhanced from an average of approximately 3 fusions per nucleus to an average of 7 fusions per nucleus.

The nuclei of neuroblasts in nbs1; mei-41RT1 double mutant third instar larvae have 2.5 times as many as nbs1 single mutants. Over 12% of the double mutant nuclei are polyploid (n = 106).

mei-41D3/mei-41RT1 partially suppresses the dorsal appendage defects of mus301094 homozygotes; 70% of eggs derived from double mutant females have wild-type dorsal appendages, 21% have fused dorsal appendages and 9% have no dorsal appendages. mei-41D3/mei-41RT1 partially suppresses the dorsal appendage defects of eggs derived from spn-Bunspecified females.

The eggshell patterning defects of eggs derived from spn-BBU/spn-BBU females are suppressed if the females also carry mei-41RT1/+ or mei-41D3/mei-41RT1.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments

mei-41RT1 and mei-41RT2 reside within 400bp of each other. Transposase induced reversion demonstrates a P-element insertion is responsible for the mutant phenotype.

The chromosome carrying mei-41RT1 is relatively stable in the absence of P\TΔ2-3 (which encodes a functional transposase), however in the presence of P\TΔ2-3 the stability of the mei-41RT1 chromosome is severely reduced. This instability is reversed if P\TSal is also present.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
References (25)