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Based on this notion, our Dlk1 conditional mutants should have elevated Notch signaling, which would suppress MyoD expression[79].
As the conditional mutants should have normal levels of circulating Dlk1 which is mainly produced by the fetal liver, our results suggest that muscle specific membrane-bound Dlk1 is important for normal myogenesis.
FLN's localization to TAC complexes suggests that PEP loss of function mutants should have similar phenotypes.
LYM1, LYM3 and CERK1 genes are essential for PGN signal transduction, so the mutants should have almost no response to soluble PGN.
Collins et al. (2014) therefore reasoned that if Corolla was a component of the SC, then corolla mutants should have high levels of both X and 4th chromosome nondisjunction (see figure 1B in Collins et al. 2014).
Yet, it is well established that DAF-2 inhibits DAF-16 and that DAF-16 is activated in daf-2 mutants, so, if DAF-16 mediates all signaling from DAF-2, daf-2 mutants should have a surplus of DA, instead of DA deficiency.
Similar(53)
Besides the inconsistency with wild type, the E1R/R4E+KCNE1 mutant should have similar "inhibition" to E1R/R4E.
Among the genes regulated by CRP there are many membrane transport proteins [ 31], so a crp E. coli mutant should have membrane alterations among other negative pleiotropic effects.
If the amino acid were not ligated to the enzyme, the mutant should have selenocystine reductase activity similar to that of the truncated enzyme (enzyme 10).
If offset univalents bias spindle rotation or if the cortex-proximal pole exerts greater pulling on univalents after rotation, then a mei-2 ct98) mei-2 ct98le mutant should have a redoublefrequency of mutantrogeny relative to him-8 alone.
The use of null knock-in alleles allows investigators to compare cells that express a SSTF, in heterozygotes, to the equivalent cells, in mutants, that "should have" expressed the SSTF.
Related(20)
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