MED25/PFT1 was first identified as a positive regulator of flowering in response to sub-optimal light conditions, and pft1 mutants display slightly longer hypocotyls in far red light and a late flowering phenotype in long days [ 16].
Conversely, the S276D mutant displayed slightly delayed translocation of p65 into the nucleus (right hand panels).
Surprisingly, though the Δppk2 mutant displayed slightly elevated ppGpp accumulation compared to WT (Figure 2A), there was no significant difference in the ppGpp accumulation either after 1 hr or 3 hr labeling.
Compared with the wt RNF4-SIM domain, the single SIM mutants displayed only slightly weaker binding to tetra-SUMO2 with KD values in the low micromolar range.
A phospho-mimetic mutant for the adjacent casein kinase I and cdk5 sites (127E/131E) did not display changes in activity (Fig. 4C and D), whereas a phospho-mimetic mutant for compound phosphorylation by both casein kinase I and cdk5 (101E/127E/131E/378E) displayed slightly enhanced autoubiquitylation activity (Fig. 4E G).
The membranes displayed slightly anisotropic membrane swelling.
Treated mice displayed slightly lower parasitemia levels (Fig. 4D).
Thus, the caf1 21, caf2 3, caf3 89, caf4 83 and caf5 mutants displayed pleiotropic, albeit slightly different, phenotypes to the cells: caffeine resistance, increased sensitivity to UV-irradiation, a reduction in fertility, lengthening of the cell cycle and some morphological aberrations [10].
Interestingly, the R301K mutant displayed a slightly higher kcat than the parent PTDH, and a more modest increase in Km for phosphite (nearly 40-fold).
Only two of ten nitrofurantoin-resistant mutants and four of ten trimethoprim-resistant mutants displayed an apparent cost of resistance.
