Microbiology

Event Date: 
Wednesday, October 30, 2013 - 18:00 - 18:15
Institution: 
UNSW
Title: 

NO signals for dispersing biofilms in clinical and industrial applications

Abstract: 

A story from science bench to bedside, or at least towards it What started as purely academic studies of the life cycle of bacterial biofilms, addressing the regulation of cell death events during late developmental stages, led to the discovery of a role for nitric oxide (NO) as a key regulator of biofilm dispersal. NO, which is a simple gas and universal biological signal, was found to be produced endogenously in mature biofilms, and trigger a signaling pathway involving the secondary messenger cyclic di-GMP, which in turn activates cellular effectors resulting in dispersal. Add-back of low levels (picomolar to nanomolar range) of NO was able to induce dispersal across various single species and mixed species biofilms. While the biofilm mode of growth confers a high level of resistance to control measures including antibiotics, exposure to NO greatly increases the efficacy of a range of antimicrobial treatments. Therefore the use of low, non-toxic concentrations of NO represents a promising strategy for the management of biofilms in medical and industrial contexts. Several NO-based technologies have been developed to control bacterial biofilms, including: (i) NO-generating compounds with short or long half-lives and safe or inert residues, (ii) novel materials and surface coatings which catalytically produce NO in situ, and (iii) novel compounds for the targeted delivery of NO to infectious biofilms during systemic treatments.

Event Date: 
Wednesday, October 30, 2013 - 19:00 - 20:00
Institution: 
USyd
Title: 

How microbial community structure is shaped

Abstract: 

 
Microbes profoundly influence biological systems. Owing to their small individual size, but extremely large populations, their influence is typically an emergent property of the microbial community.  As such understanding how microbial community structure is shaped is a generic question relevant to almost all biological systems.
A major focus of my research is the interplay between diet, gut microbiota and health. Our health is the product of interplay between many different factors with arguably three of the most important being adequate nutrition, homeostatic regulation and exclusion of foreign cells. Gut functions influence all these, but occur in the immediate proximity of a huge community of microorganisms – our gut microbiome. The gut microbiome profoundly effects our health via its contribution to and influence on gut functions.
Arguably the most significant aspect of our gut microbiome is that differences in composition matter. The contribution of our microbiome to nutrition, metabolism, gut and immune functions varies from person-to-person. Thus the clinical manifestation of many diseases will be influenced by the individual’s microbiome. Secondly, environmental or lifestyle differences such as diet and hygiene may modulate microbiome composition and thus its influence on health. This gives rise to two basic opportunities for improving healthcare. These are, using the microbiome as a metric to improve diagnosis and targeting the microbiome for therapeutic intervention. We are specifically exploring forces that shape microbial community structure in mouse and human models of with a view to developing diagnostic and intervention strategies across a range of health issues. 

Event Date: 
Wednesday, August 28, 2013 - 19:00 - 20:00
Institution: 
iThree Institute UTS
Title: 

Genome plasticity in Vibrio species – how lateral gene transfer directs niche specialisation and pathogenicity

Abstract: 

Bacteria of the Vibrio genus are abundant in aquatic environments, fulfil important nutrient cycling roles and are often found in association with marine animals such as corals, molluscs, sponges, crustaceans and fish. This diversity in niche occupation is a feature of Vibrio species and is largely (or at least in significant part) driven by lateral gene transfer (LGT). LGT is a two-step process firstly requiring physical transfer of DNA from one bacterial cell to another followed by subsequent integration of the transferred DNA into the genome thus allowing stable inheritance and expression. Numerous mechanisms for integration exist such as homologous recombination and a wide-range of diverse genetic elements such as transposons, integrative conjugative elements, prophages and integrons. Using two Vibrios species, V. rotiferianus and V. cholerae, research in our laboratory has sought to understand how mobile DNA contributes to vibrio evolution, niche specialisation and pathogenicity. In V. rotiferianus, we have been researching the integron, a genetic element that contributes up to 3% of a vibrios genome in laterally acquired mobile DNA. This region is dynamic and evolves at a faster rate than mutation. Our research has shown that this region provides the organism a mechanism for reworking surface polysaccharide affecting biofilm formation and potentially interactions with higher organisms. Furthermore, we have been researching evolution in V. cholerae isolated from Sydney estuarine waters. These isolates are pathogenic in animal models with all lacking the usual virulence factors of cholera toxin and colonisation factor tcpA and most lacking type III secretion indicating the presence of novel virulence factors. One isolate we are focussing on contains a novel 32-kb mobile element inserted into the indigenous recA but carries a unique recA with only 80% identity to other V. cholerae recA genes. Overall, our research demonstrates the plasticity of vibrio genomes and the significant contribution that LGT makes to the continuing evolution to the Vibrio genus.

REPORT
Mike Manefield

Amazing turn out for JAMS last night at the Australian Museum. Three excellent presentations from Nathan Lo (Blattabacterium genome evolution - USyd), Tom Jeffries (Sydney Harbour Microbiome - UTS) and Yit Heng Chooi (Fungal metabolite genetics and biochemistry - ANU). The audience was also on the money with probing questions reassuring the speakers that their labours are well appreciated by an elite body of microbiology professionals.

The idea of a two day microbial community analysis workshop was also re-introduced and planning for this has commenced. A call is also out for volunteers for the Australian Museum Sciecne Festival (10th August, 13th-15th August and 20th-22nd August).

Please email Mike Manefield if you're interested. As of the 1st of August, we still need around 10 more volunteers.

Event Date: 
Wednesday, July 31, 2013 - 19:00 - 19:45
Institution: 
Australian National University
Title: 

Understanding Secondary Metabolite Biosynthesis as the Key to Unlock New Chemical Diversity in Fungi – from Viridicatumtoxin to the Immunosuppressive Neosartoricin

Abstract: 

The advancement of DNA sequencing technology has unlocked an unprecedented amount of microbial genomic information. These genome sequences also revealed a large number of secondary metabolite (SM) genes in both bacteria and fungi. For filamentous fungi in particular, the number of SM gene clusters encoded in the genome are often beyond the number of compounds that are reported for individual species. This is likely attributed to the tight regulation of the SM genes by the eukaryotic fungi compared to their prokaryotic counterparts, where some SM genes are only expressed in the presence of appropriate environmental signals. Research is currently going on to uncover new methods to activate these "silent" gene clusters. However, at the same time, continuously expanding our understanding of the relationship between SM compounds, the biosynthetic genes and microbial ecology will assists us in navigating the exponentially expanding seas of genomic information in the search for new bioactive compounds. The past four years, I have been involved in the elucidation of the SM pathways for viridicatumtoxin, griseofulvin, tryptoquialanine, cytochalasins, lovastatins, echinocandin, fumagilin and azaphilones. A specific example is given here on how the investigation into the genes and enzymes involved in the biosynthesis of an interesting molecule, viridicatumtoxin, eventually leads to the discovery of a new immunosuppressive compound, neosartoricin, from the human pathogens Aspergillus fumigatus and Neosartorya fischeri.

Event Date: 
Wednesday, July 31, 2013 - 18:15 - 18:30
Institution: 
University of Technology Sydney
Title: 

The Sydney Harbour microbiome: bacterioplankton diversity and dynamics

Abstract: 

Sydney Harbour and its surrounding coast is an iconic habitat that supports a diverse ecosystem however the composition and dynamics of bacterioplankton in the system remain a major knowledge gap. The harbour and coast also provide a model system for investigating the spatiotemporal distribution of microorganisms across multiple physicochemical gradients and their response to anthropogenic input. Using next-generation DNA sequencing, we provide a comprehensive profile of microbial communities from a range of habitats inside the harbour and show strong biogeographic patterns in taxonomic composition.  Using network analysis to visualize correlations between community structure and environmental variables we have identified the key drivers of community partitioning. Combined these results lead to a more detailed understanding of the diversity and roles of bacterioplankton in Sydney Harbour and its surrounds, and provide insight into marine microbial ecology generally. 

Event Date: 
Wednesday, July 31, 2013 - 18:00 - 18:15
Institution: 
University of Sydney
Title: 

Genome evolution in Blattabacterium cuenoti

Abstract: 

In addition to harbouring intestinal symbionts, some animal species also possess intracellular symbiotic microbes. The relative contributions of gut-resident and intracellular symbionts to host metabolism, and how they coevolve are not well understood. Cockroaches and the termite Mastotermes darwiniensis present a unique opportunity to examine the evolution of spatially separated symbionts, as they harbour gut symbionts and the intracellular symbiont Blattabacterium cuenoti. The genomes of B.cuenoti from M.darwiniensis and the social wood-feeding cockroach Cryptocercus punctulatus are each missing most of the pathways for the synthesis of essential amino acids found in the genomes of relatives from non-wood-feeding hosts. Hypotheses to explain this pathway degradation include: (i) feeding on microbes present in rotting wood by ancestral hosts; (ii) the evolution of high-fidelity transfer of gut microbes via social behaviour. To test these hypotheses, we sequenced the B.cuenoti genome of a third wood-feeding species, the phylogenetically distant and non-social Panesthia angustipennis.We show that host wood-feeding does not necessarily lead to degradation of essential amino acid synthesis pathways in B.cuenoti, and argue that ancestral high-fidelity transfer of gut microbes best explains their loss in strains from M.darwiniensis and C.punctulatus.
 

Event Date: 
Wednesday, June 26, 2013 - 18:15 - 18:30
Institution: 
UWS
Title: 

How to dismantle a “Trichy” parasite: Deciphering the role Tritrichomonas foetus membrane and secreted proteins play at the host-parasite interface.

Abstract: 

 
Tritrichomonas foetus is a potent veterinary pathogen, causing bovine and feline trichomoniasis. While T. foetus is well know as a venereal pathogen of cattle, it has only recently been discovered as a pathogen of cats in which it causes chronic diarrhea. T. foetus imposes significant economic losses on the beef and dairy industries worldwide. Nonetheless, despite its prevalence, T. foetus is neglected relative to other parasites of veterinary concern. There is currently no effective treatment or vaccine and prevention of infection in cattle and relies on culling infected animals. Chemotherapy in cats is limited and, depending on the country, is either not recommended or prohibited due to limited efficacy and toxicity. These extracellular parasites secrete a range of molecules that aid in tissue destruction, nutrient acquisition and immune-evasion. Proteins expressed at the host-parasite interface (i.e. secreted and membrane proteins) are critical to promoting parasite development and survival. Our central hypothesis is that these key molecules, which mediate infections caused by T. foetus, present a target for the rational design of future treatment and control strategies.

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