PPME1

Pseudomonas aeruginosa (P. aeruginosa) stands out as a key culprit in the colonization of burn wounds, instigating grave infections of heightened severity. In this study, we have performed comparative whole genome analysis of a difficult to treat extensively drug resistant (DT-XDR) P. aeruginosa isolated from a burn patient in order to elucidate genomic diversity, molecular patterns, mechanisms and genes responsible for conferring antimicrobial resistance and virulence.

P. aeruginosa SHNIBPS206 was isolated from an infected burn wound of a critically injured burn patient. Whole genome sequencing was carried out and annotated with Prokka. Sequence type, serotype, antimicrobial resistance genes and mechanisms, virulence genes, metal resistance genes and CRISPR/Cas systems were investigated. Later, pangenome analysis was carried out to find out genomic diversity.

P. aeruginosa SHNIBPS206 (MLST 357, Serotype O11)) was resistant to 14 antibiotics including carbapenems and harboured all four classes of beta lactamase producing genes: Class A (bla_PME-1, bla_VEB-9), Class B (bla_NDM-1), Class C (bla_PDC-11) and Class D (bla_OXA-846). Mutational analysis of Porin D gave valuable insights. Several efflux pump, virulence and metal resistance genes were also detected. Pangenome analysis revealed high genomic diversity among different strains of P. aeruginosa.

To our knowledge, this is the first report of an extensively drug resistant ST 357 P. aeruginosa from Bangladesh, which is an epidemic high-risk P. aeruginosa clone. Further research and in-depth comprehensive studies are required to investigate the prevalence of such high-risk clone of P. aeruginosa in Bangladesh.

Protein phosphatase 2A (PP2A) is an essential serine/threonine protein phosphatase that belongs to the type2A protein phosphatase family with PP4 and PP6. PP2A functions as a trimeric holoenzyme, and the composition of the trimer is regulated by the methyl-esterification (methylation) of PP2A. Demethylation of PP2A is catalyzed by protein phosphatase methyl-esterase-1 (PME-1). Despite the physiological and pathophysiological importance of PME-1, the impact of changes in PME-1 expression on the transcriptome has not been reported. This study provides transcriptome data to gain a comprehensive understanding of the effects of PME-1 knockout on intracellular signaling of mouse embryonic fibroblasts. Our data showed that PME-1 suppresses inflammatory signaling, activates PI3K/Akt signaling, and promotes epithelial-mesenchymal transition.

Once deposited in the plant cell wall, pectin undergoes demethylesterification by endogenous pectin methylesterases (PMEs), which play various roles in growth and development, including defense against pathogen attacks. Pathogen PMEs can alter pectin's methylesterification pattern, increasing its susceptibility to degradation by other fungal pectinases and thus playing a critical role as virulence factors during early infection stages. To investigate the evolutionary history of PMEs in the Dothideomycetes class of fungi, we obtained genomic data from 15 orders (79 species) and added genomic data from 61 isolates of Corynespora cassiicola. Our analyses involved maximum likelihood phylogenies, gene genealogies, and selection analyses. Additionally, we measured PME gene expression levels of C. cassiicola using soybean as a host through RT-qPCR assays. We recovered 145 putative effector PMEs and 57 putative non-effector PMEs from across the Dothideomycetes. The PME gene family exhibits a small size (up to 5 members per genome) and comprises three major clades. The evolutionary patterns of the PME1 and PME2 clades were largely shaped by duplications and recurring gene retention events, while biased gene loss characterized the small-sized PME3 clade. The presence of five members in the PME gene family of C. cassiicola suggests that the family may play a key role in the evolutionary success of C. cassiicola as a polyphagous plant pathogen. The haplogroups Cc_PME1.1 and Cc_PME1.2 exhibited an accelerated rate of evolution, whereas Cc_PME2.1, Cc_PME2.2, and Cc_PME2.3 seem to be under strong purifying selective constraints. All five PME genes were expressed during infection of soybean leaves, with the highest levels during from six to eight days post-inoculation. The highest relative expression level was measured for CC_29_g7533, a member of the Cc_PME2.3 clade, while the remaining four genes had relatively lower levels of expression.