We demonstrated that, apart from SPOP WT, none of the mutants binds to AR. Accordingly, all the mutants failed to affect the steady-state levels of endogenous AR in C4-2 cells.
Overall, the emphasis will be on mutant genes that promise additional insights for the role of mutants known to affect starch synthesis and for those mutations in genes encoding enzymes that have important roles in the process.
Thus, myosin and MyBP-C CM mutants converge to affect the activation properties of the thin filament and can be analyzed by this activation paradigm.
To determine if the DNA pieces resulted from the DNA fragmentation that occurs during apoptosis, we analyzed mutants known to affect apoptosis in C. elegans (reviewed in [1], [2]).
To identify some of the molecules involved, we tested several mutants known to affect avoidance behaviour.
Comprehensive reviews about the mutants known to affect meiosis [ 6] and about the genes controlled of male gametophyte development [ 7] help to understand and clarify certain moments in this issue, but not completely.
Rather than acting in pharyngeal glands, sma-1 functions in the surrounding musculature, suggesting that pharyngeal muscles play a critical role in maintenance of gland morphology by restricting their growth, and analysis of other mutants known to affect pharyngeal muscles supports this hypothesis.
However, like nuc-1, crn-6, or crn-7 single mutants, loss of all three DNase II genes in the crn-7 crn-6; nuc-1 triple mutant fails to affect either the timing of apoptosis or the activation of apoptosis (Figure 1C).
The inability of both wt-AR expression and targeted knockdown of the endogenous mutant AR to affect the growth of E006AA cells implies that the AR signaling machinery is deficient in E006AA cells.
We next examined the ability of WT Vif and Vif mutant molecules to affect A3DE expression (Fig. 4A).To this end, we transfected HEK293T with the A3DE expression vector plus a control vector (Fig. 4A, lane 1), the expression vector for WT Vif-myc (lane 2), or one of the Vif mutant molecules (lanes 3, 4, 5, and 6).
