12/16/2014

Key Transcription Factor in Plant Senescence Regulates Chlorophyll Degradation and Abscisic Acid Biosynthesis

Summary

The timing of plant senescence can have a significant impact on the yield and quality of bioenergy feedstocks. Therefore, more knowledge is welcome on the regulation of and genes involved in plant senescence. Department of Energy BioEnergy Science Center researchers have gained new understanding of senescence in the experimentally tractable plant Arabidopsis thaliana. Chlorophyll degradation is an important part of leaf senescence, but the underlying regulatory mechanisms are largely unknown. The researchers found that the dark, excised leaves of an Arabidopsis thaliana transcription factor mutant (nap) exhibit a stay-green phenotype. This finding is correlated with lower transcript levels of several known chlorophyll degradation genes, and higher chlorophyll retention than the wild type during dark-induced senescence. Several plant hormones play a role in senescence; one of them, abscisic acid (ABA), is known to induce leaf senescence. Transcriptome coexpression analysis revealed that ABA metabolism/signaling genes were disproportionately represented among those positively correlated with expression of the NAP transcription factor. To further investigate ABA’s role in senescence and the stay-green phenotype, ABA was applied exogenously to excised NAP mutant leaves. Transcript levels of several chlorophyll degradation enzymes increased and the stay-green phenotype was suppressed. Collectively, the results show that the NAP transcription factor promotes chlorophyll degradation by enhancing transcription of the ABA biosynthesis gene, AAO3, which leads to increased levels of the senescence-inducing hormone ABA. This new understanding will be helpful in improving yields of bioenergy feedstocks by controlling senescence.

References

Yang, J., E. Worley, and M. Udvard. 2014. “A NAP-AA03 Regulatory Module Promotes Chlorophyll Degradation via ABA Biosynthesis in Arabidopsis leaves,” The Plant Cell 26, 4862–74. DOI: 10.1105/tpc.114.133769.