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Therefore, to increase our likelihood of detecting any developed resistance mutants we performed our sequence analysis on DNA samples from the earliest possible time point at which HIV-1 DNA was detected.

In order to measure the copy number of rDNA repeat in Sup mutants, we performed pulsed field gel electrophoresis and subsequent Southern blotting using 5S rRNA gene as a probe (Fig. 3a).

To test whether tissues were undergoing apoptosis in ablated mutants, we performed whole-mount TUNEL staining.

To obtain all NR2E3 mutants we performed mutagenesis according to the QuikChange®II Site-Directed Mutagenesis Kit.

To further investigate the molecular underpinning of development in the null mutants, we performed RT PCR for T/brachyury on mutant versus control embryos.

To further study the lifespan of germline-deficient mutants, we performed survival assays using both glp-4 and glp-1 mutants grown on heat-killed E. coli.

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In order to determine whether OsUBC13 could functionally complement the error-free PRR defect in the yeast ubc13 null mutant, we performed yeast killing and spontaneous mutagenesis assays.

To investigate the cytological mechanisms responsible for the pollen abortion of oslap6 mutant, we performed transverse section analysis for the anthers of oslap6 and WT.

Although the m-seps indicate that the distributions of the P-Shift scores are appreciably lower for the mutants compared with the non-mutants, we performed a permutation analysis to assess whether the observed m-seps are significant using a non-parametric approach.

To determine whether this was the case in the msh4 mutant, we performed FISH of the elongated nucleus.

To provide further evidence that kri1l is defective in cas002 mutant, we performed a rescue experiment by microinjection of synthetic wild-type kri1l mRNA into cas002 mutant embryos.

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