Murine Mfrn rescues the defects in frs zebrafish, and zebrafish mfrn complements the yeast mutant, indicating that the function of the gene may be highly conserved.
However, kcat/KM is higher with both substrates for the triple mutant, indicating that binding energy has been diverted from substrate binding to transition state stabilization.
By contrast, SRL1 and ACL1 have no expression changes in rel2 mutant, indicating that the two genes may not have functional relationship with REL2 (Fig. 9).
Gene expression in response to exogenous ABA is also delayed in abcg40 mutant, indicating that ABA transport is also involved in ABA-dependent signaling.
Compared with that of its wild-type parent, the content of Chl a, Chl b and total Chls decreased significantly in the mutant, indicating that the mutant phenotype resulted from reduced chlorophyll level.
SQDB extended lifespan in the ser-1 mutant, indicating that SQDB acts independently of serotonin signaling in prolonging lifespan.
Evidence for outer chains was obtained for the wild type strain, but not for the mutant, indicating that AfOch1 is essentially required.
The triple mutant Δeaf3Δnto1Δrpd3 was similar to the Δeaf3Δnto1 double mutant, indicating that S-phase could not be further shortened by the deletion of RPD3 (Fig. 6C).
As shown in Figure 4d, dynein could still interact with this mutant, indicating that the clathrin box alone is not sufficient for dynein binding.
Functional regulation by Cavβ subunits was rescued in the Bdel2 mutant, indicating that this part of the linker forms β-sheet.
Third, expression of CO, which is a photoperiod pathway gene, was not changed in the sr45-1 mutant, indicating that SR45 does not operate in the photoperiod pathway.
