After graduating from Sichuan University in 1984, Jinrong Peng was admitted to Shanghai Institute of Biochemistry, China's foremost institute at the time, for his masters studies. After attaining his M.Sc, he was appointed as an assistant lecturer at Fudan University, one of the China's best Universities. In 1990, he was awarded the Sino-British Friendship Scholarship to pursue his graduate studies in the United Kingdom. He received his PhD from John Innes Centre, a prestigious institute for plant molecular genetics. He was appointed as a senior scientist by Institute of Molecular Agrobiology in 1999 and jointed IMCB (from August 2002) to continue his excellent research program.

Genetic and genomic approaches to study liver initiation and development in Zebrafish
The liver is one of the largest internal organs in the body and is well-known as the main organ for maintaining homeostasis as well as the main site for detoxification. Although its role in maintaining homeostasis is well studied, liver initiation and development are poorly studied through genetic approaches, and only a handful of information has been obtained from in vitro tissue culture and tissue explantation experiments.
In recent years, zebrafish (Danio rerio) has been chosen as a model system for the study of vertebrate development. Our goal is to identify genes involved in liver initiation and development in zebrafish. We have obtained and preliminarily characterized 19 independent liver defect mutant lines in zebrafish. Our final goal is to clone these mutant genes via positional cloning with the hope to reveal how these genes are involved in controlling liver development. Four mutant genes have been cloned via map-based cloning. We are currently focusing on identifying the molecular mechanism behind the mutant phenotype observed.
In addition, a liver defect mutant caused by the viral vector insertion inserted in a novel gene named def (digestive-organ-expansion-factor) was obtained from Nancy Hopkins’ lab. Detailed molecular analysis revealed that loss-of-function of def selectively up-regulates the expression of a newly identified p53 isoform D113p53 (human counterpart D133p53) that leads to the up-regulation of cell-cycle-related genes but not apopototic-related genes to arrest the expansion growth of the major digestive organs, including liver.
Finally, combining the use of Affymetrix zebrafish genechip and in-house generated zebrafish cDNA microarrays, we obtained 129 genes that are genuinely enriched in the adult liver. 69 of these liver-enriched genes are also found to be enriched in the embryonic liver via whole-mount in situ hybridization. These 69 genes will be subjected to functional studies via morpholino-mediated gene knock-down method to understand if they are involved in the liver development. Eventually, target-selected mutagenesis (TILLING method) will be carried out to identify mutants corresponding to interesting genes selected from morpholino studies.
The combination of forward genetics and reverse genetics studies will no doubt strengthen our understanding of the molecular mechanism of the liver development. Since the fundamental molecular mechanisms of development are shared among vertebrates, the analysis of zebrafish mutants is likely to provide new information generally relevant to other classes of vertebrates.