Jai Tree

The lab is interested in how bacteria pathogens cause disease with a strong focus on understanding how non-coding RNAs control virulence gene expression. It is now apparent that the genomes of all organisms are transcribed into an array of regulatory non-coding RNAs (ncRNAs) and our major challenge now is to understand the functions of these RNA species. The lab uses a range of molecular techniques including UV-crosslinking, high throughput sequencing, RNA structure probing, and bioinformatics to understand the functions of regulatory RNAs. Regulatory RNAs and pathogenesis Our model system is the human pathogen, enterohaemorrhagic E. coli O157 (EHEC), that causes disease ranging from gastroenteritis to life treating haemolytic uremic syndrome. The later is caused by release of Shiga toxins that are expressed from bacteriophage (bacterial viruses) that have inserted into the bacterial genome. We have recently identified large numbers of non-coding RNAs that are encoded in EHEC and are seeking to identify those that regulate virulence. We anticipate that by understanding how bacteria employ ncRNAs to control gene expression and respond to stress we will be able to design interventions that limit bacterial pathogenesis and dissemination. Regulatory RNAs and antibiotic resistance Non-coding RNAs play prominent roles in controlling the composition of the bacterial cell wall and membranes. A number of ncRNAs have been shown to control intrinsic antibiotic resistance in bacterial pathogens with 'urgent' or 'serious' levels of antimicrobial resistance. Non-coding RNAs contribute to antibiotic resistance in Methicillin-resistant Staphylococcus aureus (MRSA, designated a 'serious' threat) and we are using high-through put sequencing technologies, bioinformatics, and molecular biology to identify key ncRNAs that mediate antibiotic resistance in MRSA. More information on the lab's research can be found on the Tree Lab website. Microbiology, Molecular Biology, RNA biology

Characterisation of the genetic mutation driving enhanced superantigen SpeA expression in Streptococcus pyogenes M1UK. Davies MR, Keller N, Brouwer S, Jespersen MG, Cork AJ, Hayes AJ, Pitt ME, De Oliveira DMP, Harbison-Price N, Bertolla OM, Mediati DG, Curren BF, Taiaroa G, Lacey JA, Smith HV, Fang NX, Coin LJM, Stevens K, Tong SYC, Sanderson-Smith M, Tree JJ, Irwin AD, Grimwood K, Howden BP, Jennison AV, Walker MJ. 2023. Nature Communications. 14(1):1051.