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General Information
Symbol
Dmel\Mps1ald-1
Species
D. melanogaster
Name
FlyBase ID
FBal0000408
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
ald1
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

G17671390A

Amino acid change:

R7H | Mps1-PA; R7H | Mps1-PB

Reported amino acid change:

R7H

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

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

Amino acid replacement: R7H.

A missense mutation.

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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

chromosome & oocyte (with Mps1C3)

meiosis & nuclear chromosome

meiosis & nuclear chromosome (with Df(3R)ED5780)

spindle microtubule & oocyte (with Mps1C3)

spindle pole & oocyte (with Mps1C3)

Detailed Description
Statement
Reference

ald1/aldC3 females show 8.2% nondisjunction of the X chromosome.

33% of oocytes show disorganisation of the chromosomes in ald1/aldC3 females. The oocytes also show spindle defects; 10% have frayed spindles, 14% of spindles are monopolar and 5% lack tapering at the pole.

Oocytes from ald1/Df(3R)AN6 mutant females enter anaphase prematurely. ald1/Df(3R)AN6 mutant females do not appear to reach a stable metaphase arrest. Shortly after the spindle forms the chromatin begins to separate into separate masses. This division is not always complete, and can appear aberrant. In some oocytes, the chromatin mass elongates and appears partially split, but remains connected by thin threads of DNA, or large DNA masses can even move back and forth across the spindle.

ald1/Df(3R)AN6 mutants undergo premature separation in all oocytes.

Oocytes from ald1 homozygotes enter anaphase prematurely. ald1 mutant females do not appear to reach a stable metaphase arrest

ald1 homozygotes undergo separation in nine out of 21 oocytes.

ald1 mutants show segregational defects for achiasmate homologs. The frequency of achiasmate X chromosome nondisjunction is increased more than 20-fold in FM7a/X; ald1 females, compared to FM7a/X; ald1/+ females. The frequency of nondisjunction is even greater (>70-fold higher than FM7a/X; ald1/+ females) in FM7a/X; ald1/Df(3R)ED5780 females. FM7a/X; ald1 and FM7a/X; ald1/Df(3R)ED5780 mutants also show an increased frequency of 4th chromosome nondisjunction, although this frequency is less than half that of the X chromosome. Cytological analysis shows that the X and 4th chromosome nondisjunction is due to a defective alignment of the achiasmate chromosome pairs at the metaphase plate. ald1 neuroblasts exhibit a failure of the meiotic spindle checkpoint. Following treatment with colchicine, the checkpoint of wild-type neuroblasts is activated and cells arrest in metaphase. In contrast, 20% of ald1 neuroblasts and ~5% of ald1/+ neuroblasts fail to arrest, as shown by precocious chromatid separation. FM7a/X; ald1 females show a relatively low level of chiasmate X chromosome nondisjunction (5.5% higher than FM7a/X; ald1/+ females). This frequency is higher (~20%) in FM7a/X; ald1/Df(3R)ED5780 females. ald1 and ald1/Df(3R)ED5780 oocytes have a defect in the maintenance of chiasmate connections between autosomal arms at metaphase I, leading to precocious autosomal separation. Defective ald1 metaphase plates either display two pairs of autosomes that are fully separated by wispy threads of chromatin, or a complete separation of the autosomes that creates anaphase-like figures.

Homozygous females display elevated levels of nondisjunction of X and fourth chromosomes (9.5 and 6.0% respectively); double exceptions are predominantly XX;0 and 0;44, products expected from nonhomologous disjunction; behavior of large autosomes nearly normal. Exchange frequencies normal and sex-chromosome exchange tetrads contribute to exceptional products.

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

mei-381 ; ald1/aldC3 double mutant females show 20.9% nondisjunction of the X chromosome.

mei-381 ; ald1/aldC3 double mutant females show spindle defects in the oocyte, with no spindles appearing normal; 17% have frayed spindles, 43% of spindles are monopolar, 37% lack tapering at the pole and 27% show a reduction of microtubules between the poles.

CG182124.6 fully complements the meiotic nondisjunction phenotype of ald1 mutants.

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

AxsD may be epistatic to ald1 with respect to its effect on fourth chromosomal disjunction. There is no evidence for second site noncomplementation between Axsr2 and ald1.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (11)