However, when grown in the dark the Atcrt1a crt1b double mutant did exhibit an additive phenotype compared to the Atcrt1a and crt1b single mutant parent lines (Figures 7F and G), suggesting that both AtCRT1a and CRT1b contribute to etiolated seedling growth.
However, the Nrp1 VEGF− mutant did exhibit a delay in vascular extension and a reduction in the number of arteries in the postnatal retina.
The mutant does exhibit some acclimation, however, which we attribute to the fact that high light initiates several signaling pathways in addition to 1O2 (e.g. reduced PQ pool, H2O2, O2-), to which sak1 is still capable of responding, and we have previously shown that a more general oxidative stress response can induce resistance to RB (Fischer et al., 2012).
The remaining 6 out of 21 long-lived mutants did exhibit an additional extension of maximal CLS when treated with rapamycin (supplementary material Fig. S1; p<0.05).
It was noted that all ATPalpha CJ mutants did exhibit an increased activity level upon startle stimulation but this increase was significantly less than that observed in wild-type controls.
However, a number of mutants did exhibit moderate mutator activity (reduced proofreading) yet showed wild-type levels of basal SOS expression (middle of Figure 2): G17S (dnaQ928); CLNNK; NSCLN; CLNKA; and LVFKQ.
However, the mutants did exhibit ectopic induction of hypha at the lower concentration of HU (5 mM) (Fig. 4d); this observation indicated that Sz. japonicusSJ tel1 has a role in genome maintenance at stressed replication forks.
Although R265 cna1Δ mutants were more tolerant to growth on solid medium at 37° compared with cna1Δ mutants generated from C. gattii R272, WM276, and C. neoformans H99 strains, the R265 cna1Δ mutants did exhibit a clear growth defect at 37° that was more severe than the modest impact of the calcineurin inhibitor FK506 or CsA on strain R265 growth at 37°.
Nrp1 VEGF- mutants do exhibit some of the angiogenesis phenotypes previously reported in Pan et al., 2007 and Fantin et al., 2014 such as reduced vascular extension and reduced retinal arteries at P9.
For instance, Wang et al. argued with the finding of Honjo's group, showing that cells harboring the N51A mutant did not exhibit a detectable antibody diversification18.
Cells infected with the C. jejuni wild-type strain and the capA mutant exhibited increased Erk1/2 phosphorylation compared to uninfected cells, while cells infected with the flpA mutant did not exhibit increased Erk1/2 phosphorylation.
