Joachim Messing, Dr. rer. nat., ML

September 2016

Joachim Messing is a biologist recognized for work in genomics and biotechnology. The shotgun DNA sequencing method and the M13mp/pUC/JM cloning kits made him the most frequently cited scientist in the world for the eighties. Messing made his innovations freely available, ensuring rapid advances in all life sciences. With contributions to plant genomics he focuses on raising the nutritional quality of food. Messing was born in Duisburg, Germany, in 1946, studied Pharmacy at the Free University of Berlin, and received his doctorate degree from the Ludwig Maximilian University of Munich in Biochemistry. After studies at the University of California at San Francisco and Davis, he rose through the faculty ranks at the University of Minnesota before becoming a University Professor of Molecular Biology at Rutgers and then the Director of the Waksman Institute of Microbiology, where he holds also the Waksman Chair in Molecular Genetics. He was winner of the 2013 Wolf Prize in Agriculture and the 2014 Promega Biotechnology Award. Messing, a Fellow of the American Association of the Advancement in Science and the American Academy of Microbiology, is a member of the US and the German National Academy of Sciences and the American Academy of Arts and Sciences.


Research Highlights

Besides his early work in molecular biology Messing has focused on plant genetics. His laboratory has studied in particular genes that are expressed during the development of cereal seeds. He is well known for the genomic studies of grass genomes and his laboratory has contributed to the sequencing of rice, sorghum, maize, Brachypodium, and Spirodela. These genomic sequences have permitted his laboratory to study the organization and evolution of the genes that control the supply of proteins for nutrition. More recently, his laboratory has used RNA interference to study the role of these proteins in seed development and molecular breeding. One of the new initiatives of his laboratory investigates the potential of sweet sorghum and duckweed as alternative bio-energy sources. Publications are tagged in categories of Bioenergy, Epigenetics, Genome Evolution, Genome Structure, Protein Quality, RNAi, and Shotgun DNA Sequencing. Out of 200 publications prior to 2008 only representative samples are listed.

Recent Publications

Larkins, BA, Wu Y, Song R, Messing J.  2017.  Maize seed storage proteins. Maize Kernel Development. :175-189.
Messing, J.  2017.  Does Investment in Research Always Pay Off? American Academy of Arts and Sciences Bulletin. 70(3):45-47.
Garcia, N, Li Y, Dooner HK, Messing J.  2017.  Maize defective kernel mutant generated by insertion of a Ds element in a gene encoding a highly conserved TTI2 cochaperone. Proceedings of the National Academy of Sciences of the United States of America. 114(20):5165-5170. Abstract
We have used the newly engineered transposable element Dsg to tag a gene that gives rise to a defective kernel (dek) phenotype. Dsg requires the autonomous element Ac for transposition. Upon excision, it leaves a short DNA footprint that can create in-frame and frameshift insertions in coding sequences. Therefore, we could create alleles of the tagged gene that confirmed causation of the dek phenotype by the Dsg insertion. The mutation, designated dek38-Dsg, is embryonic lethal, has a defective basal endosperm transfer (BETL) layer, and results in a smaller seed with highly underdeveloped endosperm. The maize dek38 gene encodes a TTI2 (Tel2-interacting protein 2) molecular cochaperone. In yeast and mammals, TTI2 associates with two other cochaperones, TEL2 (Telomere maintenance 2) and TTI1 (Tel2-interacting protein 1), to form the triple T complex that regulates DNA damage response. Therefore, we cloned the maize Tel2 and Tti1 homologs and showed that TEL2 can interact with both TTI1 and TTI2 in yeast two-hybrid assays. The three proteins regulate the cellular levels of phosphatidylinositol 3-kinase-related kinases (PIKKs) and localize to the cytoplasm and the nucleus, consistent with known subcellular locations of PIKKs. dek38-Dsg displays reduced pollen transmission, indicating TTI2's importance in male reproductive cell development.
Xiang, X, Wu Y, Planta J, Messing J, Leustek T.  2017.  Overexpression of serine acetyltransferase in maize leaves increases seed-specific methionine-rich zeins. Plant biotechnology journal. Abstract
Maize kernels do not contain enough of the essential sulphur-amino acid methionine (Met) to serve as a complete diet for animals, even though maize has the genetic capacity to store Met in kernels. Prior studies indicated that the availability of the sulphur (S)-amino acids may limit their incorporation into seed storage proteins. Serine acetyltransferase (SAT) is a key control point for S-assimilation leading to Cys and Met biosynthesis, and SAT overexpression is known to enhance S-assimilation without negative impact on plant growth. Therefore, we overexpressed Arabidopsis thaliana AtSAT1 in maize under control of the leaf bundle sheath cell-specific rbcS1 promoter to determine the impact on seed storage protein expression. The transgenic events exhibited up to 12-fold higher SAT activity without negative impact on growth. S-assimilation was increased in the leaves of SAT overexpressing plants, followed by higher levels of storage protein mRNA and storage proteins, particularly the 10-kDa δ-zein, during endosperm development. This zein is known to impact the level of Met stored in kernels. The elite event with the highest expression of AtSAT1 showed 1.40-fold increase in kernel Met. When fed to chickens, transgenic AtSAT1 kernels significantly increased growth rate compared with the parent maize line. The result demonstrates the efficacy of increasing maize nutritional value by SAT overexpression without apparent yield loss. Maternal overexpression of SAT in vegetative tissues was necessary for high-Met zein accumulation. Moreover, SAT overcomes the shortage of S-amino acids that limits the expression and accumulation of high-Met zeins during kernel development.