Thus, the Mmi1W112A mutant that affects Mmi1-Erh1 interaction without disrupting the termination function of Mmi1 provides a unique tool to uncouple EMC-dependent and -independent functions of Mmi1.
An orally available compound identified by high-throughput screening, the CFTR potentiator VX-770 (Ivacaftor, trade name Kalydeco), has been shown to efficiently reduce chloride levels in sweat and to improve lung function in CF patients harboring the G551D CFTR genotype, a rare class III CFTR mutant that affects only 4 5%% of CF patients [7, 8].
A third mutant that affected circadian Fe responses was hy6, defective in the main chloroplast-localized haem oxygenase, HO1, involved in phytochrome (Phy) chromophore biosynthesis from haem (Chory et al, 1989; Davis et al, 1999).
Although most mutants affecting cilial morphology or function lead to a decrease in Shh pathway function, such as seen in the IFT52, IFT57, IFT88/polaris, IFT172 and Kif3a mutants (66– 69, 72, 73), at least one mutant that affects retrograde intraflagellar transport results in activation of the Shh pathway (42).
This validates that the positive genetic selection for mutants impaired in light/carbon repression of ASN1::HPT2 enabled us to isolate an Arabidopsis mutant that affects the light/carbon regulation of genes involved in metabolism and other genes in related energy pathways.
An orally available compound identified by high-throughput screening, the CFTR potentiator VX-770 (Ivacaftor, trade name Kalydeco, Vertex Pharmaceuticals), efficiently reduces chloride levels in sweat and improves lung function in CF patients harboring the CFTR G551D genotype, a rare class III CFTR mutant that affects only 4%to5%5% of CF patients worldwide.
In contrast to previous studies, here we describe a collection of mutants that affect subpopulations of cilia.
By further challenging mutant flies with L. monocytogenes mutants, we identified subgroups of fly mutants that affect specific stages of the L. monocytogenes life cycle, exit from the vacuole, or actin-based movement.
The study of mutants that affect RNA splicing and editing provides a novel and powerful method to explain the role of specific sequences involved in these processes.
Surprisingly, the growth defect of the double ΔtreYZΔtreS double mutant was suppressed by various Arabidopsis cell wall mutants that affect xyloglucan synthesis, including an xxt1xxt2 double mutant that completely lacks xyloglucan, even though xyloglucan mutants are not more susceptible to pathogens and respond like wild-type plants to immune elicitors.
