Insertion 7bp upstream of the 3' splice junction of the first intron.
In comparison with wild-type, transgenic XpdD234N embryos in a XpdSH2137 mutant genetic background show highly enhanced death rates after ultraviolet light irradiation with a dose of 100 J/m[2].
In comparison with wild-type, transgenic XpdG47R embryos in a XpdSH2137 mutant genetic background show highly enhanced death rates after ultraviolet light irradiation with a dose of 100 J/m[2].
In comparison with wild-type, transgenic XpdG675R embryos in a XpdSH2137 mutant genetic background show highly enhanced death rates after ultraviolet light irradiation with a dose of 100 J/m[2].
Compared with wild-type, elevated cell-cycle synchrony defects are detected in transgenic XpdR601L embryos in a XpdSH2137 mutant genetic background.
Compared with wild-type, elevated cell-cycle synchrony defects are detected in transgenic XpdR683W embryos in a XpdSH2137 mutant genetic background.
Compared with wild-type, elevated cell-cycle synchrony defects are detected in transgenic XpdG47R embryos in a XpdSH2137 mutant genetic background.
Compared with wild-type, elevated cell-cycle synchrony defects are detected in transgenic XpdG675R embryos in a XpdSH2137 mutant genetic background.
Compared with wild-type, elevated cell-cycle synchrony defects are detected in transgenic XpdR112H embryos in a XpdSH2137 mutant genetic background.
Compared with wild-type, elevated cell-cycle synchrony defects are detected in transgenic XpdR722W embryos in a XpdSH2137 mutant genetic background.
Compared with wild-type, an enhanced rate of DNA loss and abnormal free centrosomes that often continue to divide in subsequent cycles is detected in transgenic XpdR683W embryos in a XpdSH2137 genetic background.
Compared with wild-type, an enhanced rate of DNA loss and abnormal free centrosomes that often continue to divide in subsequent cycles is detected in transgenic XpdG47R embryos in a XpdSH2137 genetic background.
Compared with wild-type, an enhanced rate of DNA loss and abnormal free centrosomes that often continue to divide in subsequent cycles is detected in transgenic XpdG675R embryos in a XpdSH2137 genetic background.
Compared with wild-type, an enhanced rate of DNA loss and abnormal free centrosomes that often continue to divide in subsequent cycles is detected in transgenic XpdR112H embryos in a XpdSH2137 genetic background.
Embryos derived from homozygous XpdSH2137 females expressing XpdScer\UAS.T:SV5\V5 under the control of Scer\GAL4αTub84B.PL do not hatch into larvae. 38.7% of the embryos show nuclear division defects during the nuclear division cycles. The nuclear division defects can be restricted to a small part of the embryo or may affect larger regions. The defective nuclei fail to segregate their chromatin properly and show nuclear fusions and chromatin bridges (these can be seen in interphase, late anaphase or telophase). Mitotic figures are seen in which chromosome segregation has failed to occur properly by telophase. Some of the mutant embryos have chromatin-free regions containing free centrosomes (suggesting that improperly divided nuclei have fallen into the interior of the embryo during previous cycles). Some of these extra centrosomes are seen associated with nearby nuclei. The synchronization of late syncytial division cycles is also often lost in these embryos.
Nuclear cycles 12 and 13 usually take much longer than normal in embryos derived from homozygous XpdSH2137 females expressing XpdScer\UAS.T:SV5\V5 under the control of Scer\GAL4αTub84B.PL. Delays of 50-100% are often seen at the anterior end of the embryo, while the delays at the posterior end can be much longer. The mitotic wave from the anterior pole often proceeds almost or entirely to the posterior end before the posterior mitotic wave is initiated (in contrast to wild type).
Embryos derived from homozygous XpdSH2137 females expressing XpdScer\UAS.T:SV5\V5 under the control of Scer\GAL4αTub84B.PL have a highly elevated frequency of mitotic spindles that branch out into neighbouring mitotic figures, with microtubules from one spindle "reaching over" to the neighbouring mitotic figure and appearing to attach to a chromosome.
Scer\GAL4αTub84B.PL, XpdSH2137, XpdUAS.Tag:V5 has abnormal mitotic cell cycle | maternal effect | embryonic stage phenotype, suppressible | partially by CycB[+]/CycB2
Scer\GAL4αTub84B.PL, XpdSH2137, XpdUAS.Tag:V5 has abnormal mitotic cell cycle | maternal effect | embryonic stage phenotype, suppressible | partially by Df(2R)59AB/+
XpdSH2137/Xpd[+] is a suppressor | partially of visible phenotype of Scer\GAL4GMR.PU, crbintra.UAS.Tag:MYC
XpdSH2137/Xpd[+] is a suppressor | partially of eye phenotype of Scer\GAL4GMR.PU, crbintra.UAS.Tag:MYC
One copy of XpdSH2137 strongly suppresses the small and rough eye phenotype seen when crbintra.Scer\UAS.T:Hsap\MYC is expressed under the control of Scer\GAL4GMR.PU.
The nuclear division defects seen in embryos derived from homozygous XpdSH2137 females expressing XpdScer\UAS.T:SV5\V5 under the control of Scer\GAL4αTub84B.PL are partially rescued if the females are carrying either CycB2/+ or Df(2R)59AB/+.
XpdT:SV5\V5 rescues between 1/3 and 1/5 of the expected number of XpdSH2137/Df(2R)K11 flies.
XpdSH2137 animals expressing XpdScer\UAS.T:SV5\V5 under the control of Scer\GAL4αTub84B.PL develop to the adult stage. The rescued adults do not show any morphological abnormalities and rescued males are fertile. Rescued females show normal egg production, however, while the resulting embryos initiate developmental normally, no larvae emerge from them.