How did Ding know where to look? The China native was partly acting on a hunch that started when he was a graduate student at the Australia National University in the late 1980s. There, during a lecture, he learned that the genomes of viruses infecting plants and animals are actually very similar, even though plants and animals are very different.
That, and further discussions with his mentor Adrian Gibbs, an expert on molecular evolution of viruses and a fellow of the Australian Academy of Sciences, "made me think there must be a common anti-viral mechanism in plants and animals to keep their viruses similar," he said.
Ding produced the first evidence for that hypothesis while working with Bob Symons in the Waite Institute in South Australia, studying cucumber mosaic virus, a devastating, aphid-carried disease that infects more than 1,000 plant species, including many important crops.
Using computational analytical skills learned from Gibbs, Ding discovered a small gene in the virus other scientists had overlooked. He named the gene 2b and showed that it plays an essential role in helping the virus spread within the host plant. Based on his results, and published studies on the B2 protein of Flock house virus, an insect pathogen, Ding proposed in a 1995 paper that 2b and B2 proteins act by suppressing the host's antiviral defense.
Fueled by that idea, Ding moved to Singapore in 1996 to set up his own laboratory in the Institute of Molecular Agrobiology. There, in collaboration with a British group led by RNAi-expert David Baulcombe, Ding's group discovered that the 2b protein did indeed suppress the RNAi virus-fighting properties in plants. Further, the group found that the 2b proteins of the related viruses all have the suppressor activity even though they share limited
|Contact: Iqbal Pittalwala|
University of California - Riverside