Nucleotide substitution: T?A.
Amino acid replacement: L24term.
T23273646A
T?A
L24term | ord-PA; L24term | ord-PB
L24term
When ord4/ord10 female flies with normal X chromosomes are subjected to a 4-day aging regimen (after collection of virgin females and feeding with yeast paste overnight, the virgin females are kept for 4 days in the absence of males, which results in the majority of oocytes halting in developmental progression and aging within the female abdomen, as oviposition is suppressed), sex chromosome nondisjunction is not significantly greater in aged oocytes than in non-aged oocytes.
When ord8/ord10 female flies with normal X chromosomes are subjected to a 4-day aging regimen (after collection of virgin females and feeding with yeast paste overnight, the virgin females are kept for 4 days in the absence of males, which results in the majority of oocytes halting in developmental progression and aging within the female abdomen, as oviposition is suppressed), sex chromosome nondisjunction is significantly greater in aged oocytes than in non-aged oocytes. The majority of nondisjunction events are reductional in both aged and non-aged oocytes.
Meiotic crossovers on the X chromosomes are substantially reduced in ord4/ord10 and ord8/ord10 oocytes; the total map distance is reduced to 20% or less of the wild type value.
When subjected to the aging regimen, FM7a/X ; ord4/ord10 aged oocytes show a significant increase in nondisjunction that lasted for 48 hours. Reductional nondisjunction events predominate in both aged and non-aged oocytes.
When subjected to the aging regimen, Df(1)bb158/X ; ord4/ord10 females show age-dependent nondisjunction; sex chromosome nondisjunction is significantly greater in aged oocytes than in non-aged oocytes.
When subjected to the aging regimen, In(1)dl-49/X ; ord4/ord10 females do not show age-dependent nondisjunction.
Heterochromatin pairing between the FM7a chromosome and a normal X chromosome is significantly disrupted in ord4/ord10 oocytes.
DNA double-strand breaks occur at approximately the same frequency in ord10 nuclei and are formed and repaired as in wild-type. Recovery of the ring X chromosome R(1)2 relative to a normal rod X chromosome during female meiosis is significantly lowered in ord5/ord10 (ratio of ring/rod=0.2 compared to 0.7 in wild-type) and ord6/ord10 (ratio of ring/rod=0.4 compared to 0.7 in wild-type) mutants.
Oocytes from ord10/Df(2R)3-70 mothers exhibit sister-chromatid cohesion defects. The cohesion affects are not seen until after nuclear envelope breakdown. Loss of cohesion is seen in 45% of prometaphase I figures. In addition oocytes are unable to arrest at metaphase I. and cohesion defects are obvious in 72% of oocytes that progress beyond metaphase I. Unlike in wild-type oocytes from ord10/Df(2R)3-70 fail to arrest at Metaphase I, though oocytes are sometimes seen in prometaphase I. Other effects in segregation are also seen. The level of meiotic recombination in ord10/Df(2R)3-70 oocytes is about 16% of wild-type.
Random segregation of chromosomes due to complete loss of sister chromatid cohesion. Females do not produce any oocytes arrested at metaphase I following residual exchange events.
Hemizygotes are viable and exhibit no cuticular, bristle or eye phenotypes but have reduced female fertility. Light microscope analysis of chromosomes reveal no gross abnormalities reflecting aberrant segregation during the germ-line mitotic divisions. Orcein stained testes squashes reveals loosely organised bivalents with single chromatids protruding from the chromosome mass. Staining reveals initial homologue association is not compromised severely in males. Unlike the wild-type situation, precocious separation of sister chromatid is readily apparent in males during meiosis II. Cohesion is totally absent before anaphase II and aberrant anaphase II figures with unequal polar distribution of chromatids are often seen, consistent with the production of aneuploid gametes. No metaphase II figures are observed. In the absence of ord protein (ord10 hemizygotes or ord10/ord5 transheterozygotes) sister chromatid cohesion is missing and individual chromatids segregate randomly to the poles with minimal chromosome loss.
FM7a, ord8/ord10 has abnormal meiotic cell cycle phenotype
FM7a, ord10/ord4 has abnormal meiotic cell cycle phenotype
ord10 has stage S1 oocyte | increased number phenotype, suppressible by pch2EY01788a
ord[+]/ord10 is an enhancer of oocyte | oogenesis stage S12 phenotype of IncenpQA26
ord[+]/ord10 is an enhancer of oocyte | oogenesis stage S13 phenotype of IncenpQA26
Scer\GAL4VP16.nanos.UTR, ord5/ord10, vtdGL00522 has ovary phenotype
Scer\GAL4VP16.nanos.UTR, ord5/ord10, vtdGL00522 has female germline cell phenotype
c(2)MZ0810/c(2)MEP2115, ord5/ord10 has oocyte phenotype
c(2)MZ0810/c(2)MEP2115, ord5/ord10 has chromosome | female | adult stage phenotype
SA1GL00534, Scer\GAL4VP16.nanos.UTR, ord5/ord10 has ovary phenotype
SA1GL00534, Scer\GAL4VP16.nanos.UTR, ord5/ord10 has female germline cell phenotype
IncenpQA26, ord[+]/ord10 has synaptonemal complex phenotype
IncenpQA26, ord[+]/ord10 has oocyte | oogenesis stage S14 phenotype
Expression of SAGL00534 under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 in the ord5/ord10 mutant background results in rudimentary ovaries lacking germ cells.
c(2)MEP2115/c(2)MZ0810,ord5/ord10 double mutants show defects in centromere clustering and sister chromatid cohesion (assessed by number of cid foci) in pachytene oocytes relative to controls.
Assembly of the synaptonemal complex is normal in the ovaries of IncenpQA26 ord10/IncenpQA26 females. However, these females show premature disassembly of the synaptonemal complex.
85% of stage 12 and 13 oocytes show prometaphase I configurations with separated chromosomes in IncenpQA26 ord10/IncenpQA26 females, and at stage 14, 53% of the oocytes have aberrant metaphase I chromosome configurations. The X and fourth chromosomes show a failure of bivalent biorientation.
ord10/Df(2R)3-70 is rescued by ordmNeonGreen