Dr Jai Tree

Senior Lecturer
3113, L3 East, Bioscience South E26
(+612) 9385 9142
(+612) 9385 1485

Lab: Samuels s128; Phone 9385-3869

Lab website: https://treelab.science/

Professional Experience

2015-current:  Senior Lecturer, School of BABS
2014-2015:  NHMRC Postdoctoral Researcher, Peter Doherty Institute, Uni of Melbourne
2010-2014:  Postdoctoral Researcher, Wellcome Centre for Cell Biology & The Roslin Institute, University of Edinburgh
2007-2010:  Postdoctoral Researcher, Royal (Dick) School of Veterinary Studies, University of Edinburgh

Research Contribution

My lab has an ongoing interest in how complex genetic traits such as virulence are assembled and selected in bacterial pathogens.

Transcriptional regulation of bacterial virulence
Many bacterial pathogens, including Staphylococcus, Vibrio, Salmonella spp., and E. coli have acquired the genes for pathogenesis through horizontal gene transfer. A stark example of this is Enterohaemorhaggic E. coli (EHEC), which has obtained more than a fifth of its genome (and its ability to cause disease) through acquisition of mobile genetic elements (termed pathogenicity islands or PAIs). This suggests a level of ‘plug and play’ genetics and raises the question of how this assortment of genetic material is regulated and coordinated to allow a productive virulence program.

By screening mutant libraries and analysing clinical isolates of EHEC we have identified a number of regulators acquired on PAIs that control virulence. A recent example is the prophage secretion regulator (Psr) family of transcriptional regulators that coordinates expression between independent, horizontally acquired PAIs. Psr encoding islands carry virulence proteins known as ‘effectors’ that are injected into host cells by the type 3 secretion system (T3SS). Psr was found to regulate T3SS through the acid stress response - encoded within the conserved ‘core’ genome. We speculate that coordination between the pathogenicity islands positively selects for effector secretion.

Post-transcriptional regulation of bacterial virulence 
Non-coding RNA regulation has come to the fore with the advent of RNA sequencing. It is now abundantly apparent that all forms of life transcribe RNAs that do not encode proteins (non-coding RNAs), but regulate cellular processes through a myriad of mechanisms. Bacterial pathogens produce hundreds of non-coding RNAs, however we have a poor understanding of the function of the majority of these RNAs.

UV-crosslinking and deep sequencing protein-RNA complexes (CRAC or CLIP-Seq) is a powerful technique for identifying protein interaction sites on RNAs. We have used this technique to study interactions between the ncRNA chaperone, Hfq, and the transcriptome. Using this technique, we have demonstrated that the pathogenicity islands of EHEC are rich in a class of ncRNA, termed small RNA (sRNA), and have revealed a new mechanism of ncRNA regulation. Unusally short RNAs (50-60nt) were identified that control the activity of sRNAs (as opposed to mRNAs). This new class of sRNAs have been termed ‘anti-sRNA’. We have found that anti-sRNA are required for effective growth of EHEC in bovine mucus, the environmental reservoir of EHEC, and are investigating the mechanisms behind this growth defect.

RNA has two particularly useful properties for gene regulation; it is able to adopt a huge variety of conformations that can respond to environmental cues (e.g. riboswitches and RNA thermometers), and make sequence-specific interactions with RNAs through (often limited) base pairing. We anticipate that the mechanisms adopted by ncRNAs to control gene expression in bacterial pathogens will be exceptionally diverse, and are using UV-crosslinking and deep sequencing techniques to study these processes.

Active Research Projects


Click here for Dr Tree's publications list