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Schematic of LbCpf1 and AsCpf1 DNase-dead mutants was shown in Fig. S1A.
Instead of depending on elongation stimulation, restoration of viability of dnaX dnaA double mutants was shown to result from a decrease in the efficiency of initiation.
This sequence of events is supported by a previously published report in which, the epithelial invasiveness of Fur-defective mutants was shown, in an acid-sensitive independent manner, to be lower than that of the wild-type strain [82].
We favor the latter scenario, because a general defect in COPII-dependent secretion in sar1 mutants was shown to result in tracheal tube expansion defects similar to those observed in γCOP mutants, whereas tracheal lumen fusion was not reported to be affected in COPII component mutants [2].
Translation termination in UPF1 mutants was shown to be dependent on the sequence context.
Loss of mitochondria at NMJs in Drp1 mutants was shown to affect synaptic transmission at high frequency stimulation (Verstreken et al., 2005).
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The genotypes of WT and the overexpressing mutants are shown in Fig. 5a.
In addition, four mutants are shown to significantly stabilize Raf RBD native structure.
These genes were amplified by the primers cueO-F and cueO-R, and gene mutants are shown by vertical bars.
The average heading dates of the wild type and the z3 mutants are shown by closed and open arrows, respectively.
Finally, four mutants, Sm5-V1, Sm2-V10, Sm7-V12, and Sm7-V12, were identified in the ARTP breeding process, and the TGase production of these mutants is shown in Table 3.
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