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These mutant analyses suggest that ABL1 modulates ABA and auxin responses.
Double mutant analyses suggest that PAX1 also interacts genetically with other members of the Aux/IAA family.
While mutant analyses suggest that IXB targets CESA3 and CESA6 [ 13, 14], the mode of action and specific target of TA have not yet been identified.
During wildtype embryogenesis, both genes are expressed during neuroblast delamination, and mutant analyses suggest that Snail and Worniu function in neuroblasts, around the time of division to give rise to ganglion mother cells (GMCs) [ 61].
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Our results on the cell-specific rescue, over-expression and double-mutant analyses suggest that AHO-3 acts in sensory neurons including AWC for thermotactic plasticity (Figs 3C,D, 4A F and 5A,B and Fig. S10A,B in Supporting Information).
Double-mutant analyses suggested that aho-3 acts in the same genetic pathway with odr-3 encoding G protein alpha subunit (Fig. 7C and Figs S12H, S13C and S13G in Supporting Information).
Further mutant and pharmacological analyses suggest that known players in plastid-to-nucleus signalling do not directly participate in Fe sensing.
The altered functions or defects in processing of the pre-miRNAs in the mutant alleles detected in our analyses suggest that these microRNAs may contribute to the development of schizophrenia.
These analyses suggest that W351A and Y300A mutant enzymes might be ideal candidates for oxidizing otherwise inhibitory oligosaccharides when present at high substrate concentrations.
DOI: http://dx.doi.org/10.7554/eLife.03189.018 The above analyses suggest diminished PcG activity in Scrib module mutant tissues, but do not point to a molecular mechanism.
Further analyses suggest that the changes in catalytic efficiency for mutant enzymes are correlated to structural changes within the binding site.
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