Open Close
General Information
Symbol
Dmel\ord1
Species
D. melanogaster
Name
FlyBase ID
FBal0013283
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Nucleotide change:

G23272272A

Amino acid change:

R401H | ord-PA; R401H | ord-PB

Reported amino acid change:

R401H

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: R401H.

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

ordys91/ord1 males show 26.2% non-disjunction between the X and Y chromosomes.

Meiotic recombination is reduced but not absent. Encoded protein is able to poison the activity of ord4 in males and females: negative complementation. Mutation exhibits negative complementation when in combination with ord8 in males and females, missegregation is greater in ord8/ord1 transheterozygotes than that in ord8 hemizygotes.

Transmission rate of Dp(1;f)J21A through females to progeny is 28%, mei-S3321 ord1 double mutant causes a mild reduction in transmission. mei-S3321 ord1 double mutant also decreases transmission of Dp(1;f)1B, Dp(1;f)25A and Dp(1;f)10B. mei-S3321 ord1 double mutant do not effect Dp(1;f)J21A transmission in males.

Level of chromosome missegregation in heterozygous females is 0%, levels in males and females significantly increase when transheterozygous with ord4. Also the frequency of X chromosome exchange of the transheterozygous is lower compared to ord4 homozygotes.

Primary spermatocytes in homozygous male flies show a high degree of aneuploidy. The pattern of ring canal inheritance in the meiocyte cysts is disrupted and the number of cells in each cyst is variable. In addition the cells occupying the cyst are very asynchronous in development in contrast to wild-type. Pycnotic cysts are common. There is also a high frequency of non-disjunction during gonial mitotic divisions, which involves the large autosomes more frequently than the sex chromosomes or chromosome 4. Homozygous males are defective in some aspect of the mechanism(s) that holds sister chromatids together during meiosis; the majority of sister kinetochores in prometaphaseI-metaphaseI primary spermatocytes are physically separated, and are smaller than wild-type. Testes of homozygous males are much smaller than wild-type.

In females homozygous for ord, exchange is strongly reduced. In both males and females, ord causes a dramatic increase in both reductional and equational nondisjunction as assayed genetically. In male meiosis, Goldstein observed abnormal sister-chromatid associations during prophase as well as precocious sister-chromatid separation, followed by random disjunction during anaphase I. 'The bulk of the first division misbehavior consists of sister chromatids' disjoining from one another, a process which normally occurs only during the second meiotic division' (Goldstein, 1980). ord also elevates the frequency of mitotic chromosome misbehavior (Baker et al., 1978). 'A substantial proportion of this mitotic instability can be accounted for by a hypothesis in which ord causes precocious sister-chromatid separation, followed by random disjunction, in somatic as well as germ-line cells' (Goldstein).

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

ord1/ord3 has phenotype, non-suppressible by anon-59Da3.6RR

Additional Comments
Genetic Interactions
Statement
Reference
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Fails to complement
Not rescued by
Comments
Images (0)
Mutant
Wild-type
Stocks (4)
Notes on Origin
Discoverer
Comments
Comments

Strong ord mutation.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (8)