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Homology-modelling analysis indicates that enhanced polar contacts of the 64th residue in this mutant may contribute to stabilizing the structure of the enzyme and promote the interactions between enzyme and substrate.
This suggests that the inability to express alsSD at adequate levels in a sarA mutant may contribute to its inability to form a biofilm.
Extensive aneuploidy in the bub1 mutant may contribute to a decrease in CLS.
At the molecular level, altered binding properties of the desmocollin-2a mutant may contribute to the changes in connexin43.
Therefore, increased PigU in the hfq mutant may contribute to the decrease in rpoS transcript levels and exoenzyme production.
Lower cVA production in the miR-124 mutant may contribute to the lowered intensity of aggressive behaviors observed in these flies.
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Increased metalloproteinase activity in color mutants may contribute to the augmented ability of color mutants to induce aggravated immune responses from infected larvae.
Mislocalization of these cell-cycle regulators in ess1 mutants may contribute to the cell cycle arrest phenotype previously reported.
The same mechanisms underlying extended lifespan in dwarf mutants may contribute to the longevity extension that results from CR [ 23- 25].
A potential caveat of the paraquat study is that reduced feeding rate in mutants may contribute to resistance by reducing ingestion of paraquat.
These findings suggest that tetraspanins function as components of insect septate junctions and that their upregulation in CrebA mutants may contribute to the SJ targeting of excess membrane.
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