To analyze a mechanistic link between plectin deficiency and mitochondrial alterations, we comparatively assessed mitochondrial morphology and function in whole muscle and teased muscle fibers of wild-type, MCK-Cre/cKO and plectin isoform-specific knockout mice that were lacking just one isoform (either P1b or P1d) while expressing all others.
As with antioxidant metabolites, the contributions of these enzymes to antioxidant defenses can be hard to separate from one another, but the generation of transgenic mice lacking just one antioxidant enzyme can be informative.
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Surprisingly, however, worms that lacked just one subunit were viable, despite previous evidence that AP2 requires all four subunits to be functional.
For three of the four major plectin isoforms expressed in muscle, P1d, P1b, and P1, isoform-specific knockout mouse lines were generated, which lack just one of these isoforms, while expressing all others.
As each of these 25 species lacked just one gene in the pathway, we believe that these species do synthesize purines, and that further work will reveal novel pathway variants.
This approach contrasts with previous studies where the existence of the FLO was inferred from analyzing rhythmicity in strains that lacked just one of several components of the FWO, leaving the possibility that residual or novel network interactions involving the remaining clock components could establish a temperature-responsive oscillator.
However, a substantial minority lack just one or a few genes of the pterin or pABA branches, and detailed analysis of these cases reveals several biologically significant points.
De novo NAD+ biosynthesis is essential, and lack of just one enzyme is usually lethal (Katoh et al. 2006; Lin et al. 2010; Panozzo et al. 2002).
