Obituaries Australia

Ian Buckley, 2015

ANU Archives, 1885/12899

Ian Buckley was born in Melbourne in 1925 and attended school there until drafted into the RAAF in 1943. After World War II, he studied medicine at Melbourne University, graduating in 1951, following which he held a series of hospital appointments in country Victoria and Melbourne. In 1956 Ian returned to Melbourne University Medical School to a research and teaching position in pathology. In 1962 he became a National Health and Medical Research Council (NHMRC) Research Fellow.

In 1963 he was Eleanor Roosevelt Fellow in C.M. Pomerat’s laboratory at the Pasadena Foundation for Medical Research in California, and in the following year Research Fellow in Keith Porter’s laboratory at Harvard University.

Soon after his return to Melbourne University Medical School in 1966, he was recruited by Professor Colin Courtice to join the newly formed Department of Experimental Pathology in the John Curtin School of Medical Research (JCSMR) at ANU.

Ian’s research interests initially centred on the nature of heat and burns damage to body tissues and cells. Later, he came to consider those effects of heat damage that occur at the subcellular level, particularly involving the endoplasmic reticulum (subcellular membranous network), the cytoskeleton and the motility systems of the cell at this level— microtubules and microfilaments.

Ian came to ANU because it offered attractive conditions in which to develop his research interests—adequate salary, tenure, excellent research infrastructure and research assistance, a stimulating environment among talented and collaborative colleagues, and the freedom to develop his ideas in his own way. Funding of projects by the University was generous and did not require application for the limited support available at that time within Australia.

ANU also provided study leave generously. Ian took advantage of this in 1973 to spend a year back in Keith Porter’s laboratory at Harvard, and again in 1979 when he took a year in Nobelist James Watson’s laboratory at the Cold Spring Harbour Laboratories, in New York state.

Apart from the important mentoring support provided by Colin Courtice, Ian had generous practical and moral support from people such as Jack Harding (Head Technician in Experimental Pathology), the JCSMR workshop staff generally, and two experts in electron microscopy—Colin McLachlan and his successor Lesley Maxwell.

Ian’s later work was concerned with the fundamental structural and biochemical basis of cell movement by and in non-muscle cells, particularly the movement of organelles such as mitochondria and lysosomes inside cells, as well as the motion of cellular extensions—the microvilli and so-called ‘ruffles’, which serve to move living cells over surfaces. In his studies, such movements were recorded live on movie film, or in the arrested state by electron microscopy of critical-point-dried whole cells or thin sections of resin-embedded cells. Prospective motility proteins (such as actin, myosin or dynein) were ‘labelled’ with appropriate reactants to reveal their location and distribution within cells.

Ian identifies two exemplars of his work. The first was based on the experimental technique of micro-injection of inhibitors of one or other of the known mechanical force-generating systems inside cells—the actin/ myosin (muscle-type system), and the microtubule/dynein system.

This work was done in collaboration with Dr Murray Stewart, then in CSIRO Plant Industry. Dr Stewart had the required chemical and manipulative expertise to micro-inject inhibitors such as vanadate ion (V+5) safely (without causing cell death or disruption) into various types of cultured cell. Vanadate was known to inhibit (reversibly) the interaction of dynein with the microtubules of de-membranated sperm tails and ciliated cells, i.e. in non-intact cells. Inhibition of the interaction of dynein with microtubules in intact cells should prevent force generation and thus affect the waving motion of sperm tails and cilia. What this inhibition might do to the saltatory movements of cellular organelles such as mitochondria and lysosomes was the question addressed by Ian and Dr Stewart. From this would come an answer to whether interactions between dynein and the microtubules ,which permeate the deep cytoplasm of animal cells, are the basis of organellar movement inside living cells. Would the movement of the organelles be inhibited by micro-injected vanadate ion?

Interestingly, while micro-injected vanadate immediately stopped the motion of cilia (the effect seen in non-intact cell models), it was without effect on the cytoplasmic motion of cell organelles. This lack of effect by vanadate on organelle movement was seen both in oviduct cells and in cultured connective tissue cells.

In the case of cultured beating myocardial cells, curiously, injected vanadate caused sustained contraction for some 20 seconds. However, the muscle cells’ regular contractions then resumed normally, thus confirming that in the living cell, vanadate is not a potent inhibitor of myosin ATPase, differentiating it from the dynein ATPase.

Unfortunately, at this promising point Murray Stewart left Canberra for Cambridge, UK. Ian then began the second line of his most significant work.

Reflecting on the clinical behaviour of malignant cells in tumours, and their histological characteristics (not only the loss of differentiation and excessive proliferation of these cells, but their loss of normal morphology and extensive cellular invasion of surrounding normal tissue), Ian considered the likelihood that the central characteristic of malignant transformation is closely related to an important error in normal cell developmental mechanisms, i.e. in the molecular genetic controls known to determine cell number and positions in the developmental morphology of organisms, and of their limbs and organs (including relevant specialisations) from the earliest embryonic stages through to, and including, full development and maturation. Indeed, errors in control in almost all instances are thought to arise within a single cell, resulting in virtually all malignancies being ‘monoclonal’. Ian explored the literature for evidence to this effect, which was subsequently published.

Ian Buckley’s field of expertise in medicine was the molecular and structural basis of motility in non-muscle cells, and the nature of unregulated cellular growth and invasiveness in malignancy. After his retirement from JCSMR in 1990, Ian became interested in the political and economic history of modern warfare, in which he then lectured and wrote extensively.

In the course of his career as a scientist, Ian developed a strong social awareness. Having almost been involved personally in the large-scale carnage and destruction that characterised World War II, Ian was appalled by how quickly the Americans and their Australian and other allies so quickly became mired in two further conflagrations soon after World War II: the Korean War and the Vietnam War. This set Ian to considering how so-called civilised and advanced nations become involved in wars, and whether the rationalisations offered to the citizens of the nations involved are reliable or other than self-serving on the part of political masters and their servants.

Accordingly, Ian developed an interest in military and political history, researching in particular the origins of the Boer War and World War I. After his retirement from JCSMR, these historical studies occupied him fully. He published some of his work, and often gave seminars on these and related topics.

For a period, Ian became an active member of the ANU Emeritus Faculty as Events Officer, responsible for the faculty’s monthly and popular program of talks and lectures by academics and other experts drawn from a wide range of disciplines and fields of study.

* This obituary has been adapted from an interview conducted on 23 March 2009 at the Emeritus Faculty by Peter Stewart as part of the ANU Emeritus Faculty Oral Histories Project: hdl.handle.net/1885/12899.