In this study, the impact of Leu-214 on replication capacity and

In this study, the impact of Leu-214 on replication capacity and resistance to zidovudine (ZDV) of viruses containing TAM1 or TAM2 was determined. Leu-214 decreased the growth rate of viruses bearing Tyr-215, as well as their resistance to ZDV. This observation was confirmed by structural and molecular modeling data, suggesting a regulatory role for Leu-214 in the emergence and phenotypic resistance of TAM1.”
“Sixteen strains belonging to three families of the Rhizobiales order (Bradyrhizobiaceae, Phyllobacteriaceae Ipatasertib in vitro and Rhizobiaceae) were evaluated according

their specific growth rates (mu) and the activity of intracellular alpha-esterase and beta-esterase isoenzymes. The average esterase activity of 48 isoenzymes assayed belonging to five strains with low (mu(max) = 0.08-0.12 h(-1)), four medium (mu(max), = 0.13-0.22 h(-1)) and seven high (mu(max) = 0.24-0.28 h(-1)) growth rate values were 22.1 +/- 4.3; 8.7 +/- 2.2 and 3.9 +/- 1.7 U g(-1) respectively. An inversely

proportional relationship between the activity of the whole pattern of esterases and mu(max) was found. Our results illustrate a selleck kinase inhibitor feature of intracellular esterases, ascribable in a variety of cellular functions, which might be related to characteristics mu(max) Of legume infecting bacteria.”
“me53 is a highly conserved baculovirus gene found in all lepidopteran baculoviruses that have been fully sequenced to date. The putative ME53 protein contains a zinc finger domain and has been previously described as a major early transcript. We generated selleck inhibitor an me53-null bacmid (Ac Delta me53GFP), as well as a repair virus (AcRepME53:HA-GFP) carrying me53 with a C-terminal hemagglutinin (HA) tag, under the control of its native early and late promoter elements. Sf9 and BTI-Tn-5b1 cells transfected with Ac Delta me53GFP resulted in a 3-log reduction in budded-virus (BV) production compared to both the parental Autographa californica multiple nucleopolyhedrosis virus and the repair bacmids, demonstrating that although me53 is not essential for replication, replication is compromised in its absence.

Our data also suggest that me53 does not affect DNA replication. Cell fractionation showed that ME53 is found in both the nucleus and the cytoplasm as early as 6 h postinfection. Deletion of the early transcriptional start site resulted in a 10- to 360-fold reduction of BV yield; however, deletion of the late promoter (ATAAG) resulted in a 160- to 1,000-fold reduction, suggesting that, in the context of BV production, ME53 is required both early and late in the infection cycle. Additional Western blot analysis of purified virions from the repair virus revealed that ME53:HA is associated with both BV and occlusion-derived virions. Together, these results indicate that me53, although not essential for viral replication, is required for efficient BV production.

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