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Consistently, IncE mutants with lower affinity for SNX5 can no longer be recruited to the inclusion during infection.7,8 As the abundance of effectors translocated into the host cell is often extremely low, these observations suggest that IncE binds SNX5 with an affinity higher than CI-MPR.
Interestingly, the site recognized by IncE appears to be the site used by SNX5 to recognize the cation-independent mannose-6-phosphate receptor (CI-MPR), one of the established cargo molecules for the retromer.1,7,8 Overexpression of IncE but not its mutants with lower affinity for SNX5 interfered with the transport of CI-MPR to the trans-Golgi compartment in mammalian cells.
The iaaM-OX transgenic lines with higher endogenous indole-3-acetic acid (IAA) level and IAA pre-treated wild type (WT) plants exhibited enhanced drought stress resistance, while the yuc1yuc2yuc6 triple mutants with lower endogenous IAA level showed decreased stress resistance in comparison to non-treated WT plants.
In normal conditions, RNA viruses also do not select mutants with lower than standard mutation rate.
One could speculate that the presence of ABL/BCR supports the proliferation of cells harboring BCR/ABL mutants with lower kinase activity, such as the T315I, which boasts nearly complete resistance to small molecules [35] [36].
Anti-mutator mutants, with lower than normal mutation rates, have been observed in bacteria [32], in the phage T4 [33], and in RNA viruses evolving in the presence of mutagens [34].
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Rab mutants with lowered nucleotide affinity are known to bind GEFs with high affinity, thereby trapping the active GEF in an unproductive complex [47].
Moreover, co-expression of Rinl and Rab5a or Rab22 mutants with lowered nucleotide affinity leads to a redistribution of diffusely expressed Rab5a and Rab22 to actin-positive membrane compartments.
A relatively subtle change in the HDZIPIII / KAN activity balance characteristic for the r-protein mutants, with lowered HD/ZIPIII or increased KAN activity, might not be critical for bud auxin export and activation in wild type, but might prevent buds of max2 from activating when there is a higher auxin load in the main stem.
The expression of the fruA and levD operons was at baseline in a levQ mutant and substantially decreased in a levT null mutant, with lower expression with the cognate inducers fructose or mannose, but slightly higher expression in glucose or galactose.
A common distribution was found in which a mutant sequence was present at high frequency, surrounded by a cloud of mutant with lower frequencies.
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