作者: Lakshmi Rajagopal , Anthony Vo , Aurelio Silvestroni , C. E. Rubens
DOI: 10.1111/J.1365-2958.2005.04620.X
关键词:
摘要: Group B streptococci (GBS) are the principal causal agents of human neonatal pneumonia, sepsis and meningitis. We had previously described existence a eukaryotic-type serine/threonine kinase (Stk1) phosphatase (Stp1) in GBS that regulate growth virulence pathogen. Our previous results also demonstrated these enzymes reversibly phosphorylated an inorganic pyrophosphatase. To understand role on GBS, we assessed stk1-mutants for auxotrophic requirements. In this report, describe absence (Stk1), attenuated de novo purine biosynthesis consequently arrested. During media lacking purines, intracellular G nucleotide pools (GTP, GDP GMP) significantly reduced Stk1-deficient strains, while levels A nucleotides (ATP, ADP AMP) marginally increased when compared with isogenic wild-type strain. provide evidence result from altered activity IMP utilizing enzymes, adenylosuccinate synthetase (PurA) dehydrogenase (GuaB) strains. demonstrate Stk1 Stp1 phosphorylate PurA GBS. Collectively, data indicate novel kinases regulation metabolic processes such as biosynthesis.