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To explore the possible biological roles of N-glycosylation in plant adaptive resistance to salinity stress, we cloned the STT3 genes from S. alterniflora and heterogenously expressed them in Arabidopsis mutant to observe the functional conservation.
In order to confirm the function of SaSTT3A and SaSTT3B were truly conserved with their counterparts in the phylogenetic trees, we expressed them in A. thaliana stt3a-2 mutont tobserveve the phenotypic rescue.
Schobert et al used the V49A mutant to observe the N' intermediate with illumination at room temperature at pH 5.6.
The patch nucleation rate is low (less than 1 seed.μm−2.hour−1) which explains the necessity of a polymerization-activated mutant to observe the same assemblies by EM in previous studies (Henne et al., 2012).
The PksEI14-catalyzed reaction described above was conducted in D2O (with the more catalytically proficient Tyr185Phe mutant) to observe whether a solvent-supplied deuteron would label the γ-carbon in the product, (E -4-deutero-hex-3-enyl- S-pantE -4-deutero-hex-3-enyl-
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We introduced these transgenes into wild type and uev-1 mutants to observe in their ventral cord neurites the subcellular localization of the proteins they encode.
However, a high level of functional redundancy among the paralogues probably exists, and it may therefore be necessary to combine mutants to observe the desired effect.
In order to assess the function of these three constructs in planta, we expressed them in the A. thaliana hma2 hma4 double knockout mutant [12] to observe their effect on the Zn deficiency phenotype.
Recently it was shown that AtHMA2 expressed under its own promoter was able to rescue the Zn deficiency phenotype and Cd transport defect of the hma2 hmutanttont to levels observed in the single hma4 mutant [15].
Although we observed a wide range of reactivity across the series of mutants evaluated, we were most pleased to observe a mutant that reacted completely, D72C, and one that gave no reaction (within experimental error), N69C, as this paved the way to appraise the site-selective dual modification strategy discussed.
Transgenic over-expression of human mutant genes has been extensively used to generate mouse models for human neurodegenerative disorders due to the need of over-expressing enough amount of the mutant protein in order to observe a phenotype.
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