Mrunmay Kumar Giri
Articles written in Journal of Biosciences
Volume 38 Issue 3 September 2013 pp 583-592 Articles
Senescence is a highly regulated process accompanied by changes in gene expression. While the mRNA levels of most genes decline, the mRNA levels of specific genes (senescence associated genes, SAGs) increase during senescence.
Volume 42 Issue 3 September 2017 pp 501-508 Article
Arabidopsis MYC2 (AtMYC2) is a bHLH class transcription factor that mediates light-dependent seedling development,disease defence, JA and ABA signalling. AtMYC2 gene modulates hypocotyl elongation and expression of chlorophyll A/Bbinding protein 1 (CAB1) and rubisco small subunit protein1 (RBCS1) under blue light. The atmyc2 mutants are resistantagainst virulent bacterial pathogens. MYC2 orthologues from several crop plants have been characterized. The rice geneOs10g42430 has been referred earlier as OsMYC2 and has been shown to promote expression of JA-inducible genes.However, the role of OsMYC2 in seedling development under ABA, dark or light of specific wavelengths was not known.It was also not known whether OsMYC2 complements AtMYC2 function in Arabidopsis. We show here that expression ofOsMYC2 in the atmyc2 mutant of Arabidopsis complements the blue-light-mediated defects in hypocotyl elongation andexpression of CAB1 and RBCS1. We generated multiple transgenic rice lines for over-expression and RNAi-mediatedsuppression of OsMYC2. In agreement with AtMYC2 function, OsMYC2 over-expression and RNAi lines showedenhanced and suppressed seedling growth compared to WT plants respectively under blue light, and showed little effectunder white light or dark. In agreement with the negative regulatory role of AtMYC2 in disease defence, the RNAi linesshowed enhanced resistance against bacterial pathogen Xanthomonas oryzae pv oryzae. However, in contrast to AtMYC2function, OsMYC2 influences seedling development under red light and show no effect in ABA-mediated seed germination.Thus, the results suggest evolutionarily conserved as well as the distinct role of OsMYC2 in comparison with AtMYC2.
Volume 44 | Issue 3
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