Sentence examples for mutants were assessed from inspiring English sources

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(A) The phosphorylated threonine and serine residues shown in Fig. 1D were mutated to alanine, and Atg31 mutants with single mutations or multiple mutations in various combinations, as well as Atg31 deletion mutants, were assessed for autophagy activity under nitrogen starvation conditions.

The normalized conductance-voltage relationship of mutants were assessed in the absence and presence of 2 µM BmK IT2 with a 25 ms-PP.

While ephrinB2−/− mice display defective intersomitic vessel patterning that can be attributed to vascular specific ephrinB2 [44], these mutants were assessed after the DLAV had formed.

The altered phenotypes of the mutants were assessed by comparison to the parental strain MR-1 with the OmniLog PM bioinformatics software.

When these mutants were assessed for reversion after 3-days incubation on KB plates at 28°C, no SM-LR were detected except when WS-12 was incubated at 28°C on KB plates (%WS: WS-4, WS-13 & WS-12 on LB, 100%; WS-12 on KB, 67%; cf. WS, 28%), indicating that the maladaptive WS character on agar plates must be the over-expression of cellulose.

Therefore, the associations between Gαq and these mutants were assessed.

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The secondary structure of the mutants was assessed by far-ultraviolet (UV) circular dichroism (CD) spectroscopy.

The virulence of 20 in-frame deletion mutants and 37 transposon mutants was assessed.

In vivo virulence attenuation of ΔsimA and ΔscpI mutants was assessed in juvenile (∼15 g) HSB (Morone chrysops×Morone saxatilis) as previously described [7].

The virulence of SCHU S4 mutants was assessed by following the outcome of infection after intradermal administration of graded doses of bacteria.

Because (i) unbalanced metabolism might be sensed by cells as a stress, (ii) some nutritional stresses interfere with DNA replication [14], [15] and (iii) osmotic shocks can suppress Ts mutations in division and replication genes [29] [31], the effect of various stresses on the Ts phenotype of replication mutants was assessed.

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