Microbial geneticistContents
Introduction
Summary of career
Extract from interview and focus questions
Activities
Keywords
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Professor Jim Pittard was interviewed in 2011 for the Interviews with Australian scientists series. By viewing the interviews in this series, or reading the transcripts and extracts, your students can begin to appreciate Australia's contribution to the growth of scientific knowledge and view science as a human endeavour. These interviews specifically tie into the Australian Curriculum sub-strand ‘Nature and development of science’.
The following summary of Professor Pittard’s career sets the context for the extract chosen for these teachers’ notes. The extract discusses the dawning of our understanding of the regulation of gene expression in bacteria. Use the focus questions that accompany the extract to promote discussion among your students.
Alfred James (Jim) Pittard was born in Ballarat in 1932. He completed secondary school at the Ballarat Church of England Grammar School in 1949. Pittard then enrolled in a diploma of pharmacy at the Victorian College of Pharmacy (1950-54), where he was apprenticed firstly to Cornell’s Chemist in Ballarat and then a pharmacy in Brighton, Melbourne. After graduation, Pittard worked for a year as a relieving chemist in rural Victoria before enrolling in a bachelor of science degree at the University of Melbourne (1956-58). He then completed a master’s degree (1959-60), again at the University of Melbourne.
Pittard was awarded a Fulbright scholarship in 1960, which took him to the University of California, Berkley. A year later, Pittard’s PhD supervisor moved to Yale University, and he followed. Pittard’s PhD degree was awarded from Yale in 1963. He remained in the USA on a US Public Health Services post-doctoral fellowship for another year before returning to Australia. Pittard spent the remainder of his career in the department of microbiology at the University of Melbourne, where he was appointed firstly as a lecturer (1964-66), then senior lecturer (1966-70) and finally professor (1970-1997). Pittard’s research work was mainly focused on the genetic control of aromatic amino acid biosynthesis and transport and the control of plasmid replication. During this time he was also involved with the increasing problems of gene technology regulation. Pittard was made professor emeritus at the University of Melbourne upon his retirement in 1998.
Professor Pittard has received numerous awards recognising his scientific work and his contribution to the scientific community including; a DSc degree from the University of Melbourne (1968), the David Syme Research prize (1969), the Halford (1981) and Rubbo (1989) Orator from the Australian Society for Microbiology, the Lemberg medal from the Australian Society for Biochemistry and Molecular Biology (1991), honorary life membership to the Australian Society for Microbiology (1998), an honorary doctorate of medicine from the University of Melbourne (1999) and membership to the Order of Australia (2001).
Professor Pittard was elected to the fellowship of the Australian Academy of Science in 1974 and served as a member of Council (1978-79), its vice president (1980-81) and secretary (Biological Sciences) (1994-98).
Operon model of gene regulation
When you returned to take up your position at Melbourne, how did you and why did you choose the particular research projects that you did?
Okay. In 1961, Jacob and Monod published a big paper in the Journal of Molecular Biology, talking about genetic analysis of regulatory mechanisms in bacteria. It was a paper in which they described the operon model about gene regulation. It was a very important paper. It created a paradigm shift in the way that people thought about how genes were expressed and regulated in bacteria. In their model, what they postulated was that there were two new genetic elements that one had to consider. The first one they called a ‘regulator gene’ or ‘repressor gene’. They postulated that this made something – they weren’t sure whether it was RNA or protein – which was expressed in the cytoplasm of the cell. They thought that that repressor was then able to attach itself to the second genetic element, which they called an ‘operator’. The operator was always located right next to the genes that were being controlled. So here is the model. There is a gene somewhere in the chromosome. It makes something called a ‘repressor’, which binds on the operator and stops those genes from being expressed.
The next part of the model is that small molecules, like lactose or tryptophan, can combine with specific repressors and change their activity. In the case of the lac operon the genes are switched on in the presence of lactose. So the model said, ‘The repressor binds the operator and stops it expressing’, but when lactose is there, that binds the repressor and inactivates it so that you get it switched on. In the case of the tryptophan pathway, the tryptophan genes were switched off by tryptophan. So they simply modified the model to say, ‘The tryptophan repressor is unable to act until the tryptophan combines with it. Then, when the tryptophan combines with it, it sits on the operator and switches things off.’ So this was their model. Once that was published, people all around the world went rushing off to their own systems to apply this theory to see whether it applied to their system – and I guess I was one of those.
An edited transcript of the full interview can be found at http://www.science.org.au/scientists/interviews/p/pittard.html.
Focus questions
Select activities that are most appropriate for your lesson plan or add your own. These activities align with the Australian Curriculum strands ‘Science Understanding’, ‘Science as a Human Endeavour’ and ‘Science Inquiry Skills’, as well as the New South Wales syllabus Stage 5 Science outcome 5.8.2 and Stage 6 Biology outcome 9.3.3. You can also encourage students to identify key issues in the preceding extract and devise their own questions or topics for discussion.
bacteria
chromosome
cytoplasm
gene expression
lactose
operator
operon
regulator gene
repressor gene
RNA
tryptophan
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