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Pros mutant GMCs fail to commit to a differentiated, neuronal fate: these mutant cells have prolonged expression of neuroblast markers and inappropriately continue to divide [ 34].
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Hence, Hem/Kette/Nap1 mutant GMCs display symmetric, rather than asymmetric division.
The short answer is that pros mutant GMCs do not transcribe mγ-lacZ but continue to divide and thus dilute out mγ−lacZ, resulting in high level mγ−lacZ specifically in the parental neuroblasts.
We have also denounced the GMC's 2004 decision about David Southall ("GMC Fails Child Protection", Pediatrics 2007).
As will be discussed below, actively dividing mutant neuroblasts fail to generate GMCs, resulting in the inappropriate accumulation of daughter neuroblasts at the expense of neurons.
However, expression of MCUD260A mutant or MCUE263A mutant failed to exaggerate oxidative stress-induced apoptosis (Fig. 4B).
Inset in (B ) is a fama mutant GMC at 10-dpg.
Basal synaptic transmission is largely normal in Drp1 mutant flies, but during intense stimulation mutants fail to maintain normal neurotransmission.
Marf mutants also fail to maintain proper synaptic transmission at NMJs upon repetitive stimulation, similar to Drp1 fission mutants.
GMCs are made in fama mutants, but they fail to progress into GCs and instead continue dividing while maintaining expression of earlier fate markers (Ohashi-Ito and Bergmann, 2006) and; this failure to make GCs results in seedling lethality (Ohashi-Ito and Bergmann, 2006) and.
3) In pros mutants GMCs are de-differentiated into NBs, and hence express NB markers, e.g. Dpn.
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