Amino acid replacement: Q520term.
C15384654T
C?T
Q520term | SRPK-PA; Q520term | SRPK-PB; Q363term | SRPK-PC; Q520term | SRPK-PD; Q520term | SRPK-PE
Q520term
Homozygotes are sterile, but fully viable without any obvious morphological defects.
Homozygous female germline clones show abnormal karyosome morphology.
The normal spherical karyosome morphology is often disrupted in SRPK129-09/Df(2R)ED2436 oocytes (79% at stage 6). The karyosome is often deformed, with one or more lobes extending from a mass of chromosomes. In other cases, chromosomes appear separated into multiple masses. Chromosomes sometimes appear to be extensively attached to the nuclear envelope. The karyosome defects are first seen from stage 3 and progressively worsen during oogenesis. Heterochromatin clustering is disrupted in the majority of karyosomes, even those with relatively normal morphology. The chromatin morphology of nurse and follicle cells is normal.
Meiotic spindles of mature SRPK129-09/Df(2R)ED2436 oocytes are severely defective: only residual microtubules are seen and a proper bipolar spindle structure does not form. In 43% of cases, no or only a few short stubs of microtubules are associated with the chromosomes, in 33% of the cases one or a few longer microtubules are seen and in 23% of cases a partially organised structure is formed.
SRPK129-09/Df(2R)ED2436 has karyosome phenotype, non-suppressible by lokp6/lokp6
lokp6 does not rescue the karyosome defects seen in SRPK129-09/Df(2R)ED2436 mutant oocytes.
Df(2R)Exel9015/SRPK129-09 is rescued by SRPK+tCH322-130M04
SRPK+tCH322-130M04 fully rescues the sterility and cytological defects of SRPK129-09/Df(2R)Exel9015 mutants.