Mutant age3Δ cells have a severe defect in filament formation under several different hyphal growth conditions.
For example, the knockout mutants of GAMYB in rice showed a severe defect in spikelet development, particularly in anther and pollen development (Kaneko et al. 2004).
However, the distinct pattern of mutant Tdp1 activity evident in yeast cells, suggests a more severe defect in Tdp1H432N-catalyzed resofution of 3′ phospho-adducts.
Consistent with the roles for these cytokines in Treg differentiation in the thymus, in mice with a T cell-specific deficiency in STAT5 expression a severe defect in Treg development was observed (Burchill et al., 2007).
In contrast, the pri2(C417A, C474A, C474A) mutant permanently arrested with a G1 DNA content after being released from G1 at 37°C, indicative of a severe defect in initiation of DNA replication.
Decreased transcription in neurons was coupled with a significant reduction in nascent protein synthesis and lack of MECP2 was manifested as a severe defect in the activity of the AKT/mTOR pathway.
Accordingly, TGFβ1-deficient mice display a severe defect in LC, but not in DC, development [21].
Studies have determined that MyD88-deficient mice display a severe defect in host defense against B. burgdorferi infection [48], [49].
Deletion of Uch37 resulted in prenatal lethality in mice associated with severe defect in embryonic brain development.
However, we found that OBF-1 knockout mice have a severe defect in granuloma formation at five weeks after infection.
ICOS−/− mice have been shown to have a severe defect in germinal center formation and serum IgE levels [24].
