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Three of the mutants presented a conditional-lethal phenotype in vitro.

However, 10 of the mutants (designated AM 1 10, meaning Adhesion or invasion defective Mutants) presented a higher than 50 % reduction in adherence in comparison to the adherence observed in the parent strain (Fig. 2).

Cytological analysis revealed that esk1 mutants presented a strong irx phenotype in roots, hypocotyls and stems (Figure 6).

Upon IPTG induction, both SmpB and SsrA conditional mutants presented a slightly higher growth rate when compared with the wild type strain (for SmpB, see Fig. 2).

The cortex of Pafah1b1+/−;Vldlr−/− double mutants also appear fairly normal, however, that of Pafah1b1+/− Apoer2−/− double mutants presented a severe abnormality similar to the cortical layer inversion typically seen in Reln−/−, Dab1−/− or Apoer2−/−;Vldlr−/− mutants (Fig. 5).

Furthermore, all mutants presented a particular set of active TNF-R1 downstream pathways.

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Unexpectedly, the other class of Bug22 mutants presented an even more severe phenotype.

Because of their large numbers, embryo-defective mutants present a special challenge for saturation mutagenesis.

The emergence of HBsAg mutants presents a challenge to HBV screening programs.

In S. cerevisiae, cda1 mutants present a more diffuse chitosan layer, while their surface layer remains intact.

Arabidopsis thaliana drb2 mutants present a 2 to 10 fold increase in RdDM associated p4-siRNA ([ 50] and Figure  1a) again suggesting that plant DRB2 is involved in regulating small RNA biogenesis and is therefore a regulator of RdDM.

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