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To solve the problem, a novel atmospheric and room temperature plasma mutation method was employed to generate mutants which can grow in the defined medium.
Mutants which can bind ATP, but are unable to hydrolyze, are functionally similar to a situation of DnaA binding to ATPγS.
We noticed an increased amount of EvpC in the periplasm compared to the cytoplasm in these mutants which can be attributed to the failure in secretion.
To demonstrate the effectiveness of this approach in discovering synergistic interactions among microbes, we tested it with a synthetic model system consisting of cross-feeding E. coli mutants, which can be used to mimic various compositions of natural microbial communities.
Our matrix approximation model decomposes the original double-mutant fitness matrix into separate components, representing variability across the array and query mutants, which can be utilized for estimating and correcting the single-mutant fitness effects, respectively.
The results indirectly explain why it is an advantage for bacteria to maintain QS systems that can cross-talk among different species, and conversely, why certain QS mutants which can be abundant in isolated niches, cannot spread and hence remain localized.
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Here, we chose the eRF1 mutant, which can selectively enhance Uaa incorporation in response to the amber codon without increasing the readthrough of the opal and ochre codons.
Furthermore, it has been recently shown that unusually dense biofilms are produced by a Staphylococcus aureus mutant which can no longer secrete its main thermonuclease [13].
Moreover, while a wild-type version of mammalian Hsp90α complements the budding yeast [19], [21], a Hsp90αΔ35 mutant, which can be considered intermediate between the two afore-mentioned yeast mutants, is severely defective for complementation (Morag McLean and DP, unpublished results).
To understand the pathogenesis of this novel virus in pregnancy, we analyze the chemokine and cytokine profiles, viral load and histopathological changes in placental cell line and BALB/c mice infected by the wild type pandemic influenza A(H1N1) 2009 virus, which is a clinical isolate from a patient with mild disease, and a D222G mutant, which can cause severe clinical outcome.
To avoid formation of mixed disulfides between Prx1 and Trx1 we used the Prx1-Cys52Ser active site mutant, which can still interact with p66CH2CB (see above).
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