Every splash is different; Eureka Prize finalists; junk DNA

Bulletins, Media bulletins

The 2013 Eureka Prizes finalists have discovered:

  • Better bulls emit less methane (Armidale)
  • How to use car tyres to make steel (Sydney/Newcastle)
  • The causes and effects of catastrophic firestorms (Sydney/Canberra)
  • How bats can help us treat deadly diseases (Geelong)

They’ve invented:

  • A hypodermic camera to guide surgeons (Perth)
  • A bionic eye to proof-of-concept stage (Melbourne/Sydney)
  • Nanotechnologies to deliver drugs to their targets (Melbourne)

They’ve revealed:

  • The sinister effects of micro-plastics in the oceans (Sydney)
  • How to personalise leukaemia therapy (Sydney)
  • How to slow the progression of Duchenne muscular dystrophy (Melbourne)
  • The mysteries of locust swarming (Sydney)

The 2013 Australian Museum Eureka Prizes finalists were released this morning.

Congratulations to the 100 finalists who are competing for 17 prizes worth $170,000.

Read about these and the many other achievements of the 2013 Australian Museum Eureka Prizes finalists at australianmuseum.net.au/eureka

Also revealed today:  top ten stunning science photographs for 2013

The images showcase everything from cicadas to fluid mechanics. They will be published today on the Australian Museum and New Scientist websites, and are also available for publication.

“Science is not just about deep insights and impressive data. It’s also beautiful and inspiring. The photographs entered into the New Scientist Eureka Prize for Science Photography illustrate science in all its beauty and wonder.” Michael Slezak, Australasia Reporter, New Scientist.

The winner of the prize will be announced in the presence of 700 science, government, cultural and media leaders at Sydney Town Hall on Wednesday 4 September 2013.

If you’d like the high-resolution versions of any of the finalists’ images, contact aj@scienceinpublic.com.au or call 03 9398 1416.

The three finalists are:

 eureka_cicada Elma Kearney, Sydney NSW, Growth of fungus, Paecilomyces cicadae: This ascomycetous fungus is an endoparasite of underground cicada nymphs. Infection begins when ingested spores germinate and invade the nymph, inhibiting protein synthesis (by cordycepin) and replacing internal organs with mycelia. At maturity, the fungal fruiting bodies (stromata) grow from the killed host and produce white spores.
 Imaris Snapshot Louisa Windus, Brisbane Qld, Chemokine receptor expression on prostate cancer cells in 3D culture: Utilising immune-cytochemical procedures, chemokine receptor CXCR4 (green fluorescence) expression can be visualised on the membrane of lymph-derived prostate cancer associated tumour cells (LNCaP) grown in a 3D matrix. The nucleus of each cell can be seen (red fluorescence). Over 180 z planes were acquired by confocal microscopy to reconstruct the image.
 Father's Role Richard Wylie, Safety Beach Vic, Fatherhood, Fatherhood: The Weedy Seadragon, Phyllopteryx taeniolatus, is endemic to sub-temperate and temperate Australian waters and is listed by the IUCN as a Near Threatened species. This individual showcases not only the beauty and majesty of these unique creatures but also their biologically diverse methods of reproduction in the marine environment. The female seadragon transfers fertilised eggs to the male, who then incubates them until the fully formed young hatch approximately eight weeks later.

The highly commended entries are:

  • Gary Cranitch, South Brisbane QLD, Green turtle
  • Jason Edwards, Collingwood Vic, A tale of two deaths – the poacher and the virus
  • Stuart Hirth, Brisbane QLD, Fluid mechanics
  • Ian Baguley, Westmead NSW, Emergence
  • Helen Lambert, Moonee Beach NSW, Rampant webs
  • Dr Michael Lovelace and Professor Tailoi Chan-Ling, Sydney NSW, The dawn of neurodevelopment
  • Phred Petersen, Melbourne Vic, Liquid lace

All images are now online here.

Sydney scientists have figured out how ‘junk DNA’ can control cell development

How ‘junk DNA’ can control cell development

Researchers from the Gene and Stem Cell Therapy Program at Sydney’s Centenary Institute have confirmed that, far from being “junk”, the 97 per cent of human DNA that does not encode instructions for making proteins can play a significant role in controlling cell development.

And in doing so, the researchers have unravelled a previously unknown mechanism for regulating the activity of genes, increasing our understanding of the way cells develop and opening the way to new possibilities for therapy.

Using the latest gene sequencing techniques and sophisticated computer analysis, a research group led by Professor John Rasko AO and including Centenary’s Head of Bioinformatics, Dr William Ritchie, has shown how particular white blood cells use non-coding DNA to regulate the activity of a group of genes that determines their shape and function. The work is published today in the scientific journal Cell.

“This discovery, involving what was previously referred to as “junk”, opens up a new level of gene expression control that could also play a role in the development of many other tissue types,” Rasko says. “Our observations were quite surprising and they open entirely new avenues for potential treatments in diverse diseases including cancers and leukaemias.

The researchers reached their conclusions through studying introns-non-coding sequences which are located inside genes.

As part of the normal process of generating proteins from DNA, the code for constructing a particular protein is printed off as a strip of genetic material known as messenger RNA (mRNA). It is this strip of mRNA which carries the instructions for making the protein from the gene in the nucleus to the protein factories or ribosomes in the body of the cell.

But these mRNA strips need to be processed before they can be used as protein blueprints. Typically, any non-coding introns must be cut out to produce the final sequence for a functional protein. Many of the introns also include a short sequence-known as the stop codon-which, if left in, stops protein construction altogether. Retention of the intron can also stimulate a cellular mechanism which breaks up the mRNA containing it.

Dr Ritchie was able to develop a computer program to sort out mRNA strips retaining introns from those which did not. Using this technique the lead molecular biologist of the team, Dr Justin Wong, found that mRNA strips from many dozens of genes involved in white blood cell function were prone to intron retention and consequent break down. This was related to the levels of the enzymes needed to chop out the intron. Unless the intron is excised, functional protein products are never produced from these genes. Dr Jeff Holst in the team went a step further to show how this mechanism works in living bone marrow.

So the researchers propose intron retention as an efficient means of controlling the activity of many genes. “In fact, it takes less energy to break up strips of mRNA, than to control gene activity in other ways,” says Rasko. “This may well be a previously-overlooked general mechanism for gene regulation with implications for disease causation and possible therapies in the future.”

Background information is online at  http://www.scienceinpublic.com.au/centenary/junkdna

Media contacts:

Using genes to counter rust

Lee-Hickey-smallSafeguarding an important food crop-and the world’s beer supply Embargo and press call 10:00am Monday 5 August: 151 Iseppi Road, Bowenville, Queensland

  • On-site – farmers’ crop of barley infected with leaf rust
  • Lee Hickey, University of Queensland geneticist and John Agnew,Chair of the Northern Region Barley Advisory Committee will be available for comment.

An international study led by a Queensland scientist has found a way to better safeguard an important food crop-and the world’s beer supply.

The study, led by University of Queensland geneticist Dr Lee Hickey, successfully identified a gene that protects barley against leaf rust – a disease that hit Queensland farmers in 2010 and could destroy almost a third of the national crop.

Call me for details – 0417 131 977, niall@scienceinpublic.com.au