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The HCF-1N-D1, and HCF-1N-D2 mutants lack the D2 and D1 segments, respectively.
Rough (R) Brucella mutants lack the LPS immunodominant N-formylperosamine O-polysaccharide (O-PS) and are attenuated.
Kif3a mutants lack the Shh-dependent ventral neural types, but do not have axis duplications, defects in ventral morphogenesis or anterior neural truncations (Figure 1 and 2).
A major question in the menin field is the link between missense point mutations and their loss of various menin functions— in particular, some but not all of these mutants lack the ability to interact with KMT2A/KMT2D [12].
We previously showed that two positive regulators, VtrA and VtrB, are essential for expression of these genes and that vtrA- and vtrB-null mutants lack the capacity to induce fluid accumulation in vivo [23].
The fact that viral DNA replication of C4 deficient BSCTV mutants equaled well to that of wild type BSCTV in agro-inoculated leaves and protoplasts (Fig. 3), but not in newly emerged leaves of infected plants (Fig.2), indicating that the C4 deficient BSCTV mutants lack the capacity of viral DNA movement rather than replication.
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Engineered RSV mutants lacking the ability to secrete G are thus promising vaccine candidates.
VP35 mutants lacking the coiled-coil motif or possessing a mutation designed to disrupt coiled-coil function were defective in oligomerization, as deduced by co-immunoprecipitation studies.
Attempts to generate new vaccines by obtaining mutants lacking the lipopolysaccharide O-polysaccharide, in purine metabolism or in Brucella type IV secretion system have not been successful.
We have previously shown that QPM is elevated and that the leading-strand bias is lost in mutants lacking the major 3′ ssDNA exonucleases, ExoI and ExoVII.
We further characterized these and two earlier KO mutants lacking the immediate-early18 kDa protein (FV3-Δ18K) or the truncated viral homolog of eIF-2α (FV3-ΔvIF-2α).
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