Knockout mutants

REINTANZ, B., LEHNEN, M., REICHELT, M., GERSHENZON, J., KOWALCZYK, M., SANDBERG, G, GODDE, M., UHL, R., PALME, K., bus, a bushy Arabidopsis CYP79F1 knockout mutant with abolished synthesis of short chain aliphatic glucosinolates, Plant Cell, 2000,13, 351-367. 

Sassom-Corsi I m very excited by the experiment that involved transplanting the normal SCN into the double Cry knockout mutants (Sujino et al 2003). This could tell us a lot about the relationship between the SCN masking and the entrainment of the other tissues. 

In 2004, Strasser et al. generated a xylT knockout mutant that no longer produced [3(1,2)-linked xylosyltransferase, and nfucTA andfucTB double knockout mutant that was unable to produce a(l,3)-fucosyltransferase, in... 

After ppkl inactivation, the knockout mutants show no growth defects when compared with the parent strain. One of the remarkable defects in these mutants was the loss of motility (Rashid and Kornberg, 2000 Rashid et al, 2000a,b). A low-residual polyphosphate kinase activity was detected in these mutants (Zago et al., 1999) and attributed to the activity of the ppkl gene (Zhang et al., 2002). However, one cannot exclude the existence of other pathways of PolyP synthesis in this bacterium. 

Studies with knockout mutant mice lacking one or another of the retinoid receptors suggest that there is some degree of redundancy or overlap between the receptor subtypes, and that RARy is especiallyimportant in the teratogenic actions of retinoids (Section 2.5.1.1 Mark et al., 1999 Maden, 2000) ... 

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