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Paul M Sharp

Publications and source records attributed to Paul M Sharp.

4 recordsLinked to original sources
PubMed2025

Plasmodium falciparum CyRPA Glycan Binding Does Not Explain Adaptation to Humans.

The human malaria parasite Plasmodium falciparum evolved from a parasite that infects gorillas, termed Plasmodium praefalciparum. The sialic acids on glycans on the surface of erythrocytes differ between humans and other apes. It has recently been shown that the P. falciparum cysteine-rich protective antigen (PfCyRPA) binds human sialoglycans as an essential step in the erythrocyte invasion pathway, while that of the chimpanzee parasite, Plasmodium reichenowi has affinities matching ape glycans. Two amino acid changes, at sites 154 and 209, were shown to be sufficient to switch glycan binding preferences and inferred to reflect adaptation of P. falciparum to humans. However, we show that sites 154 and 209 are identical in P. falciparum and P. praefalciparum, with no other differences located in or near the CyRPA glycan binding sites. Thus, the gorilla precursor appears to have already been preadapted to bind human sialoglycans.

Plasmodium falciparum↗
PubMed2000

Absence of translationally selected synonymous codon usage bias in Helicobacter pylori.

Synonymous codon usage in the complete genome of Helicobacter pylori was investigated. The moderate A+T-richness of the genome (G+C=39 mol%) is reflected in the overall synonymous codon usage but the frequencies of some codons cannot be explained by simple mutational biases. A low level of heterogeneity among genes was observed, but this does not appear to be due to varying mutational bias or translational selection. Some of the heterogeneity was due to amino acid composition variation among the encoded proteins, and some may be attributable to recent acquisition of genes from other species. Since Hel. pylori codon usage is not dominated by biased mutation patterns, the absence of evidence for translationally mediated selection among synonymous codons is striking. This has implications with regard to the life history of this species, and in particular suggests that Hel. pylori strains are not subject to periods of competitive exponential growth. Despite the lack of selected codon usage, base composition immediately after the translation initiation site is skewed, consistent with selection against secondary structure formation in this region.

Codon↗
PubMed1996

Codon usage in the Mycobacterium tuberculosis complex.

The usage of alternative synonymous codons in Mycobacterium tuberculosis (and M. bovis) genes has been investigated. This species is a member of the high-G+C Gram-positive bacteria, with a genomic G+C content around 65 mol%. This G+C-richness is reflected in a strong bias towards C- and G-ending codons for every amino acid: overall, the G+C content at the third positions of codons is 83%. However, there is significant variation in codon usage patterns among genes, which appears to be associated with gene expression level. From the variation among genes, putative optimal codons were identified for 15 amino acids. The degree of bias towards optimal codons in an M. tuberculosis gene is correlated with that in homologues from Escherichia coli and Bacillus subtilis. The set of selectively favoured codons seems to be quite highly conserved between M. tuberculosis and another high-G+C Gram-positive bacterium, Corynebacterium glutamicum, even though the genome and overall codon usage of the latter are much less G+C-rich.

Bacillus subtilis↗