Once referred to as an "orphan crop" grown mainly by poor farmers, pigeonpea is now joining the world's league of major food crops with the completion of its genome sequence. The completed genome sequence of pigeonpea is featured as an advance online publication on November 6, 2011 on the website of the journal Nature Biotechnology. The paper provides an overview of the structure and function of the genes that define the pigeonpea plant. It also reveals clues on how the genomic sequence can be useful to crop improvement for sustainable food production particularly in the marginal environments of Asia and sub-Saharan Africa. Years of genome analysis by a global research partnership led by the International Crops Research Institute for the Semi-Arid Tropics (ICRISAT) based in Hyderabad, India have resulted in the identification of 48,680 pigeonpea genes. A couple of hundreds of these genes were found unique to the crop in terms of drought tolerance, an important trait that can be transferred to other similar crops like soybean, cowpea, or common bean that belong to the same family. In the fight against poverty and hunger amid the threat of climate change, highly nutritious, drought-tolerant crops are the best bets for smallholder farmers in marginal environments to survive and improve their livelihoods. Pigeonpea, grown on about 5 million hectares in Asia, sub-Saharan Africa, and South-Central America, is a very important food legume for millions of the poor in the semi-arid regions of the world. Known as the "poor people's meat" because of its high protein content, it provides a well-balanced diet when accompanied with cereals. "The mapping of the pigeonpea genome is a breakthrough that could not have come at a better time.
Working with lab cultures and mice, Johns Hopkins scientists have found that a strain of the common gut pathogen Bacteroides fragilis causes colon inflammation and increases activity of a gene called spermine oxidase (SMO) in the intestine. The effect is to expose the gut to hydrogen peroxide – the caustic, germ-fighting substance found in many medicine cabinets -- and cause DNA damage, contributing to the formation of colon tumors, say the scientists. "Our data suggest that the SMO gene and its products may be one of the few good targets we have discovered for chemoprevention," says Dr. Robert Casero, professor of oncology at the Johns Hopkins Kimmel Cancer Center. In a study, Casero and his colleagues introduced B. fragilis to two colon cell lines and measured SMO gene activity. In both cell lines, SMO gene activity increased two to four times higher than in cells not exposed to the bacteria. The scientists also observed similar increases in enzymes produced by the SMO gene. The scientists successfully prevented DNA damage in these cells by blocking SMO enzyme activity with a compound called MDL 72527. The Johns Hopkins team also tested their observations in a mouse model, created by Hopkins infectious disease specialist Dr. Cynthia Sears to develop colon tumors. Mice exposed to the bacteria had similar increases in SMO. Mice treated with MDL 72527 had far fewer tumors and lower levels of colon inflammation than untreated mice. Results of the experiments were published on September 13, 2011 in the Proceedings of the National Academy of Sciences. Dr. Casero says hydrogen peroxide can freely distribute through and into other cells. "It roams around, and can damage the DNA in cells," he says. Rising levels of hydrogen peroxide and DNA damage in the colon are clear steps to tumor development, says Dr.