Cdk5α20C originates from the imprecise excision of the P{lacW}P100 insertion and it deletes about 90% of the Cdk5α coding region, including all sequences required for binding to and activating the Cdk5 product.
Cdk5α20C/Df(2L)p35-C2 adults at young age exhibit similar number of Mushroom Body (MB) neurons and negative gravitaxis abilities while at old age they exhibit a significant decrease in the number of MB neurons and in their negative gravitaxis abilities compared to controls. Cdk5α20C/Df(2L)p35-C2 adults retaining the most motor function at middle age (as assayed by wall climbing) tend to have more remaining MB neurons than the feeblest flies.
Cdk5α20C/Df(2L)p35-C2 adults are more susceptible to oxidative stress (induced by feeding with paraquat or hydrogen peroxide) compared to controls.
Cdk5α20C/Df(2L)p35-C2 transheterozygous adults display significantly reduced adult lifespan and aged adults display more severe neurodegenerative phenotype (compromised tissue integrity particularly in the mushroom body) relative to control flies of comparable physiological age (= at equivalent stage of population mortality) but this effect is not due to either increased apoptosis or necrosis. The aged mutant adults however accumulate more autophagosomal organelles relative to controls. Cdk5α20C/Df(2L)p35-C2 adult also display significantly reduced survival rate upon starvation.
Single-cell Cdk5α20C MARCM clones in the adult mushroom body initially display very low frequency of morphological abnormalities compared to controls but in aged flies show gross swelling of the proximal region of the axon in all three classes of adult Kenyon cells.
Approximately 50% of Cdk5α20C mutant embryos lacking both maternal and zygotic Cdk5α exhibit motor nerve axonal aberrations and guidance errors at modest expressivity. These defects include overextended intersegmental nerves, missing dorsal "a" branch of segmental nerves without the lateral branch being affected, missing "b" branch of intersegmental nerves and stalled transverse nerves. Adult Cdk5α20C mutants exhibit progressive loss of motor coordination.
The lifespan of Cdk5α20C or Cdk5α20C/Df(2L)J77 flies is reduced by about one third relative to controls.
Cdk5α20C has abnormal neuroanatomy | embryonic stage phenotype, non-enhanceable by Cdk5K33A.UAS.Tag:FLAG/Scer\GAL4unspecified
Cdk5α20C has abnormal neuroanatomy | embryonic stage phenotype, non-suppressible by Cdk5K33A.UAS.Tag:FLAG/Scer\GAL4unspecified
Cdk5α20C is a non-enhancer of abnormal neuroanatomy | embryonic stage phenotype of Cdk5K33A.UAS.Tag:FLAG, Scer\GAL4unspecified
Cdk5α20C/Df(2L)p35-C2 is a suppressor of increased cell death phenotype of Scer\GAL4GMR.PF, ninaEG69D.UAS
Cdk5α20C is a non-suppressor of abnormal neuroanatomy | embryonic stage phenotype of Cdk5K33A.UAS.Tag:FLAG, Scer\GAL4unspecified
Cdk5α20C has motor neuron | embryonic stage phenotype, non-enhanceable by Cdk5K33A.UAS.Tag:FLAG/Scer\GAL4unspecified
Cdk5α20C has motor neuron | embryonic stage phenotype, non-suppressible by Cdk5K33A.UAS.Tag:FLAG/Scer\GAL4unspecified
Cdk5α20C is a non-enhancer of motor neuron | embryonic stage phenotype of Cdk5K33A.UAS.Tag:FLAG, Scer\GAL4unspecified
Cdk5α20C/Df(2L)p35-C2 is a suppressor of eye disc phenotype of Scer\GAL4GMR.PF, ninaEG69D.UAS
Cdk5α20C is a non-suppressor of motor neuron | embryonic stage phenotype of Cdk5K33A.UAS.Tag:FLAG, Scer\GAL4unspecified
The massive apoptosis seen in the larval eye discs of animals expressing ninaEG69D.Scer\UAS under the control of Scer\GAL4GMR.PF is suppressed by Cdk5α20C/Df(2L)p35-C2.
The motonerve defect phenotype of Cdk5α20C mutant embryos is not significantly different from the phenotype observed in Cdk5α20C mutant embryos also expressing Cdk5K33A.Scer\UAS.T:Zzzz\FLAG, a dominant negative form of Cdk5.
Cdk5α20C/Df(2L)p35-C2 is rescued by Cdk5α+t5.5
Cdk5α20C is rescued by Cdk5α+t5.5
Cdk5α20C is rescued by Cdk5α+t5.5
The age-progressive neurodegeneration (particularly in the mushroom body of the central brain) is rescued by combination with Cdk5α+t5.5.