Molecular Genetics and Genomics

, Volume 282, Issue 1, pp 65–81

A mitogen-activated protein kinase gene, AhMPK3 of peanut: molecular cloning, genomic organization, and heterologous expression conferring resistance against Spodoptera litura in tobacco


  • Koppolu Raja Rajesh Kumar
    • Department of Plant SciencesUniversity of Hyderabad
  • Tantravahi Srinivasan
    • Department of Plant SciencesUniversity of Hyderabad
    • Department of Plant SciencesUniversity of Hyderabad
Original Paper

DOI: 10.1007/s00438-009-0446-6

Cite this article as:
Kumar, K.R.R., Srinivasan, T. & Kirti, P.B. Mol Genet Genomics (2009) 282: 65. doi:10.1007/s00438-009-0446-6


Mitogen-activated protein kinase cascade plays a very important role in plant signal transduction mechanism. A full length cDNA of 1,514 bp length, corresponding to a mitogen-activated protein kinase gene was cloned from peanut (Arachis hypogaea). Based on its high homology with Arabidopsis AtMPK3, the cDNA was designated as AhMPK3. It carried an open reading frame of 1,113 bp encoding a 371 amino acid polypeptide. AhMPK3 bears TEY motif in its activation loop and belongs to the A1 subgroup of MAPK family. Southern blot analysis revealed that AhMPK3 exists in two copies in peanut genome and its structural organization revealed well-conserved nature of these signaling components across different species. AhMPK3 when transiently expressed in tobacco leaves was found to localize in both nucleus and cytoplasm. Transgenic tobacco plants ectopically expressing AhMPK3 exhibited enhanced resistance to first and second instar larvae of Spodoptera litura and constitutively higher transcript levels of defense response genes like PR1a, PR1b, LOX1, PIII etc. Apart from this when wounded, transgenic plants accumulated high levels of PIII and PR1b transcripts rapidly compared to wild type indicating the occurrence of a priming phenomenon.


Arachis hypogaea MAPK Transgenic tobacco Herbivore resistance Protease inhibitor-II

Supplementary material

438_2009_446_MOESM1_ESM.pdf (1.2 mb)
Supplementary material 1 (PDF 1.23 MB)

Copyright information

© Springer-Verlag 2009