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Homozygous miro2 plants showed no apparent mutant phenotypes, suggesting that MIRO2 plays no important role during plant development and that MIRO2 apparently is not functionally redundant to MIRO1.
Second, HR abolition only partially rescues smc5/6 mutant phenotypes, suggesting a poorly understood HR-independent function.
Introduction of both human Cdc14A and Cdc14B into budding or fission yeast, rescues the respective cdc14 yeast mutant phenotypes, suggesting some functional conservation between these phosphatases [ 56,57].
Single, double, and triple mutants established using T-DNA insertion mutants reveal synergistic mutant phenotypes, suggesting a similar function of these three LRX genes.
The replacement of the coding sequence of TGF-β1 with TGF-β3 and TGF-β3 with TGF-β1 led to only partial rescue of the mutant phenotypes, suggesting that intrinsic differences between them contribute to the requirement of each in vivo.
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The mutant phenotypes suggest a function for Dorsal, Dif and Relish in repression of the neural fate.
Conversely, mutant phenotypes suggest a role for CUC genes in leaf polarity [ 11].
The mutant phenotypes suggest that these residues may play a similar role of phosphate stabilization during the phosphate elimination reaction.
Thus, the strong correlation of WHSC1 and LIS1 mutant phenotypes suggests that both might function in the same pathway.
Although, the two corresponding genes show high sequence similarity and an indistinguishable expression pattern in leaves [ 12], their mutant phenotypes suggest different modes of action.
Although the molecular function of AMP1 is not known, loss-of-function mutant phenotypes suggest that it restricts shoot meristematic growth [ 70, 114].
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