Furthermore, tie-2 mutants became less resistant to bleeding after VE-cadherin knockdown.
The mutant phenotype therefore becomes less competitive, with the result that the error threshold decreases.
A complementary approach would be to examine how RuBisCO packing changes under conditions where the pyrenoid becomes less organized, including mutant strains (Thyssen et al., 2003; Ma et al., 2011), elevated levels of atmospheric CO2 (Rawat et al., 1996; Borkhsenious et al., 1998), and during RuBisCO aggregation in newly divided cells at dawn (Mitchell et al., 2014).
Inactivation of CovRS was also observed at phenotypic level: the mutant strains became less virulent compared to the parental wild-type strain [9].
Therefore, the morphological differences in the conidial cell wall architecture between resting wild-type and pksP mutant conidia become less important due to the loss of the masking rodlet/melanin layer during germination.
It could be predicted given that inactivation of other S. agalactiae TCSs (CovS/CovR, DltR/DltS, RgfA/RgfC) resulted in the changes of virulent properties, however, in all these studies the mutant strains became less virulent compared to the wild-type strains [8] [12].
However, several exceptions are noted, and it becomes less predictable for mutants with lower aggregation propensities.
On the contrary, for oligomeric MPs the stability of a mutant increases as the solvation free energy of a mutated monomer becomes less favorable, indicating that the oligomeric MP mutant would be stabilized in solution due to the reduced desolvation cost for oligomerization.
Similarly, the phosphomimetic Apaf-1 mutant is more susceptible to 14-3-3ε-dependent 14-3-3ε-dependent 14-3-3ε-dependent 14-3-3ε-dependent to the presence of Cc.
For a mutant Chlorella algae it was recently shown [ 39] that gene expression becomes less sensitive to the presence of high D2O concentrations by the overexpression of certain heat shock proteins (Hsp60 and Hsp70).
