Sleep, reading key to playtime

EDITH COWAN UNIVERSITY

Structured activities, rather than TV, are most likely to have an impact on the amount of time a child spends in play, new research has found. Results from the ECU Play Project found that a child who spent an extra hour a day sleeping and being read to was more likely to engage in an additional 30 minutes of unstructured play per day. Unstructured play is important for the cognitive, emotional, and social development of children. Through play, children learn about sharing, decision-making, resolving conflict, and abstract thinking. ECU School of Psychology and Social Science lecturer, Dr. Bronwyn Harman, is the lead researcher in The Play Project. She said the research emphasises the importance of a balance in activities for a child’s optimal health. “There has been a long-held belief in the importance of the three ‘R's: reading, writing and arithmetic. We contend the fourth ‘’R’—recreation—is as equally important,” she said. The Play Project results came from quantitative research conducted in 2010 with parents of four year old children. A total of 564 participants were included in the survey. The study showed that four year olds spent, on average: 1.88 hours per day on television; 1 hour per day reading; 3 hours per day playing; and 10.35 hours per day sleeping. The research found that children who spent an hour a day at day care and an hour a day in structured activities such as dancing lessons or sports were less likely to participate in unstructured play. However, Dr Harman said the results should not be interpreted as a criticism of day care. “Day care and television both have their place in raising healthy children. This research emphasizes and reinforces the importance of balance in activities for optimal health and positive outcomes for Australian four year olds.” Editor's Note: Original news release can be found here.

What splits twins apart

GARVAN INSTITUTE

“The aim of our study was to understand what role genetics plays in determining who we are, versus the role of environmental factors." Image: jfairone/iStockphoto Identical twins have identical genomes, but that is where it stops. There are subtle differences in their personalities, how they look, how they act and in their susceptibility to disease. How can this be? It all depends on how the “epigenome” is modified by the environment, say scientists from Sydney’s Garvan Institute of Medical Research and Queensland Medical Research Institute, who have just completed an 8-year study involving 512 adolescent twins (128 identical twin pairs, as well as 128 non-identical twin pairs), with an average age of 14.15 years. More specifically, it depends on exactly how particular parts of the genome are affected by ‘methylation’, or the attachment of hydrocarbon molecules - ‘methyl groups’, that literally change the voice of the genome, silencing some genes and amplifying others. Garvan epigeneticists Dr Marcel Coolen and Professor Susan Clark focused on the methylation profiles of a group of ‘imprinted’ genes that are important in the control of growth during early development. They found differences in the methylation profiles of these imprinted genes, even in genetically identical twins. It is these changes, they say, that probably give rise to differences we observe in identical twins. Their findings are published in the International journal PLoS One, now online. “The aim of our study was to understand what role genetics plays in determining who we are, versus the role of environmental factors,” said project leader Professor Susan Clark. “We compared genetically related people with genetically identical people, seeing how closely their methylation patterns matched.” “Our findings support the hypothesis that changes in methylation reflect the interplay between the environment and genetics.” “We showed that methylation patterns are exquisitely inherited, and so the methylation patterns of identical twins are still very similar to each other. This demonstrated that the DNA sequence does instruct the methylation pattern. When that methylation pattern changes, however, it gives rise to potential changes in phenotype, or who we are.” “This is one of the largest studies ever undertaken of this sort, and these are challenging studies, so having proof of principle is important.” “We now have evidence that changes in methylation patterns occur in genetically identical people and therefore these changes can potentially change disease susceptibility.  The next step will be to examine twins that are discordant for a particular disease – such as Type 2 diabetes. In those cases, we will be looking for discordance in methylation of the key genes.” Editor's Note: Original news release can be found here.

Pro-survival proteins shift shapes

WALTER AND ELIZA HALL INSTITUTE OF MEDICAL RESEARCH

The structural change found in Bcl-w had not previously been reported for the pro-survival proteins. Image: cdascher/iStockphoto Researchers from the Walter and Eliza Hall Institute have found a structural surprise in a type of protein that encourages cell survival, raising interesting questions about how the proteins function to influence programmed cell death. Programmed cell death, or apoptosis, is a natural process in which cells are instructed to die by members of the Bcl-2 family of proteins. It is important for controlling cell numbers and destroying defective or unwanted cells, but is also involved in the development of some cancers such as leukaemia and breast cancer in which the cells have an oversupply of pro-survival proteins, resisting signals that tell them to die. Dr Doug Fairlie, Dr Erinna Lee, and Professor Peter Colman from the institute’s Structural Biology division have shown that a pro-survival protein called Bcl-w can adopt a surprising structure unlike that seen in any other Bcl-2 family protein to date. The results were published today in the journal Structure. “We determined the structure of an unusual form of Bcl-w, a pro-survival protein discovered here at the institute,” Dr Fairlie said. “Unexpectedly, we found that, structurally, Bcl-w was able to change its shape significantly. Such a change had not previously been reported for the pro-survival proteins.” Researchers at the institute have spent many years studying the proteins involved in programmed cell death. Programmed cell death is controlled by pro-survival molecules, which stop cells from dying, and pro-death molecules, which instruct cells to die. “It is well known, from biochemical analyses, that these proteins have to change shape in order to function, but we don’t know how that shape change occurs or what it looks like,” Dr Fairlie said. “A number of our structural biologists are working on solving this particular problem.” Dr Lee said the research team was able to show that, with respect to Bcl-w at least, some of these shape changes can affect the protein’s function, perhaps in a negative way. “It could be a way of regulating what these proteins do within a cell, or it could be an inherent structural difference particular to the Bcl-w protein that makes it behave slightly differently to other pro-survival proteins,” she said. “We’re still trying to understand exactly what that means for the field.” Dr Fairlie said the research gave some idea of the types of changes these proteins can undergo, something that is not well understood. “Bcl-w is an interesting case because it does not seem to be associated with tumour growth and resilience to chemotherapy agents to the same extent as other pro-survival proteins. It may be that Bcl-w, unlike other Bcl-2 proteins and demonstrated in our structure, has evolved an inherent structural flexibility that restricts its pro-survival activity, which could explain why it is not often implicated in tumour development,” he said. “It will be particularly interesting to see whether the types of structural changes we see in Bcl-w also happen with the pro-death proteins, which would tell us a lot more about how these proteins work to kill a cell,” he said. The research involved Mr Marco Evangelista, Ms Anne Pettikiriarachchi and Dr Grant Dewson from the institute, as well as researchers at The Bio21 Institute. This work was supported by the Australian Research Council, National Health and Medical Research Council, Australian Cancer Research Foundation, Leukemia & Lymphoma Society (US), Leukaemia Foundation of Australia and the Victorian Government Editor's Note: Original news release can be found here.