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We find that mab-9 expression in unc-37 mutants is also elevated in DA motor neurons, consistent with known roles for UNC-37 as a co-repressor with UNC-4.
Alternatively, an elevated down-regulation of mitochondrial degradation (e. g., by autophagy or mitophagy) in the mutants is also possible.
The notion that oxidative damage is, at most, mildly increased in mitochondrial SOD mutants is also consistent with the limited biomarker data available in the literature.
The lifespan extension of mth mutants is also dependent upon genetic background and sex, and the reduced fecundity of mth mutants was only revealed under exposure to environmental stress [13].
As the FtsZ mutants are not affected by MinC overexpression in vivo, we wanted to test whether the polymerization activity of the mutants is also less sensitive to the presence of MinC in vitro.
We also observed that the Arf/p53 module responds normally in senescing MEFs unlike that in immortalized MEFs (Supplementary Fig. S8), suggesting that the selective pressure of mutants is also coupled with acquiring immortality and tetraploidy development.
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Two more fadR super-repressor mutants were also discussed.
The relative activity of purified mutants were also shown.
The germination rate of the mutants was also different.
Exemplary mutants were also produced and compared to native protein.
Ability to produce nitrate nonutilising (nit) mutants was also assayed.
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