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Pratt, N.

Publications and source records attributed to Pratt, N..

2 recordsLinked to original sources

Genome evolution and convergent innovation in the carnivorous plant Sarracenia purpurea

The repeated evolution of certain complex traits raises a fundamental question of how genomes generate ecological novelty while preserving developmental stability. Carnivorous pitcher plants, which modify a core organ of plant performance, the leaf, exemplify this challenge, yet the genomic basis of their convergent evolution has not been resolved. We present a chromosome-scale genome assembly for Sarracenia purpurea and analyze it alongside eight additional angiosperms spanning its parent clade Ericales and several other carnivorous lineages. The genome reveals extensive syntenic duplicate blocks arising from ancient polyploidy events, with diffuse, alternating dominant and recessive segments interleaved along chromosomes. Dominant regions are biased toward retained copies of dosage-sensitive regulatory genes, including AGO1, BRX, GATA11, ETC1 and RCD1. These genes highlight a conserved regulatory scaffold associated with leaf morphogenesis, including epidermal differentiation, auxin-mediated patterning, and redox-integrated coordination. By contrast, tandem gene duplications preferentially accumulate in structurally labile genomic regions and constitute a complementary, rapidly evolving component of the genome, enriched for ecological effector functions, including detoxification, glutathione-mediated redox buffering, antifungal pathways, and cuticle modification activities. Comparative union-based functional analyses across four carnivorous taxa reveal convergent recruitment of oxidative, transport, microbial-interaction, and cell-wall processes during independent trap evolution. Transcriptomic data confirm consistent activation of these pathways in pitchers. These findings demonstrate that complex traits arise through a genome-wide partitioning between polyploidy-derived, conserved developmental regulation and tandem-driven ecological specialization, here partitioning leaf architectural control from rapidly evolving functions associated with pitfall-based prey capture.

genomics↗

Gastrointestinal carriage is a major reservoir of K. pneumoniae infection in intensive care patients

BackgroundKlebsiella pneumoniae is an opportunistic pathogen and a leading cause of hospital-associated (HA) infections. Patients in intensive care units (ICUs) are particularly at risk, and outbreaks are frequently reported in ICUs. K. pneumoniae is also part of the healthy human microbiome, providing a potential reservoir for HA infection. However, the frequency of K. pneumoniae gut colonization and its contribution to HA infections are not well characterized.\n\nMethodsWe conducted one-year prospective cohort study of ICU patients. Participants (n=498) were screened for rectal and throat carriage of K. pneumoniae shortly after admission, and clinical information was extracted from hospital records.K. pneumoniae isolated from screening swabs and clinical diagnostic samples were characterized using whole genome sequencing. Genomic and epidemiological data were combined to identify likely transmission events.\n\nResults and ConclusionsK. pneumoniae carriage frequencies were estimated at 6% (95% CI, 3%-8%) amongst ICU patients admitted direct from the community, and 19% (95% CI, 14% - 51%) amongst those who had recent contact with healthcare. Gut colonisation on admission was significantly associated with subsequent K. pneumoniae infection (infection risk 16% vs 3%, OR=6.9, p<0.001), and genome data indicated a match between carriage and infection isolates in most patients. Five likely transmission chains were identified, resulting in six infections (12% of K. pneumoniae infections in ICU). In contrast, 49% of K. pneumoniae infections were caused by a strain that was unique to the patient, and 48% of patients with K. pneumoniae infections who participated in screening were positive for prior colonisation. These data confirm K. pneumoniae colonisation is a significant risk factor for subsequent infection in ICU, and indicate that half of all K. pneumoniae infections result from patients own microbiota. Screening for colonisation on admission could limit risk of infection in the colonised patient and others.

microbiology↗