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Pollen grains from BET11/12 mutants show reduced pollen tube growth in vivo but no developmental defects before germination.
Consequently, loss of function Sh mutants show reduced sleep and increased arousal.
This is supported by the fact that several of the mitochondrial mutants show reduced GFP-Atg8a levels, consistent with increased autophagic turnover of this fusion protein.
Nor did any of the mutants show reduced cell binding.
Additionally, the mutants show reduced pollen production and disturbed ovule development, causing female sterility [ 35, 36].
Although Fgf23 −/− /VDRΔ/Δ and Kl −/− /VDRΔ/Δ mutants show reduced NCC expression and increased urinary Na+ excretion, they do not develop a typical Gitelman's syndrome.
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Marcheva et al. found that phase of oscillation of islet genes involved in growth, glucose metabolism and insulin signaling is delayed in circadian mutant mice, and both Clock and Bmal1 mutants show reduce insulin secretion, and impaired glucose tolerance [ 47].
Consistent with these observations, Mmi1Y97A and Mmi1F99A mutants showed reduced affinities for Erh1 (Supplementary Table 1).
Interestingly, mnb1 mutants showed reduced interaction between Endo and dynamin (Fig. 5c,d).
We found that BR receptor loss-of-function mutants showed reduced hydrotropic responses compared to WT plants.
Mutants showed reduced metabolic rates and altered metabolite patterns compared to wild-type.
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