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Role of NAC transcription factors in plant senescence

Fachliche Zuordnung Pflanzenphysiologie
Förderung Förderung von 2009 bis 2015
Projektkennung Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 46691270
 

Zusammenfassung der Projektergebnisse

The execution of senescence is accompanied by massive transcriptional reprogramming, whereby NAC transcription factors (TFs) play crucial roles as regulators of gene expression during senescence. Within FOR948 we studied the roles of several NAC TFs for plant senescence, using Arabidopsis thaliana as model. Our results show that the various NACs control largely different sets of target genes and, hence, different physiological pathways relevant to the induction and execution of senescence. Notably, while most senescence-enhanced NAC genes appear to encode positive regulators of senescence (e.g. ORE1, ORS1, ATAF1, SHYG), others function as negative regulators (e.g. JUB1). More specifically, we made the following observations: ORE1 positively affects senescence by directly binding to the promoters of a number of well-known senescence-associated genes (SAGs), including e.g. BFN1, SAG29, and SINA1. Other groups showed direct binding of ORE1 to ACS2 (involved in ethylene biosynthesis) and various chlorophyll catabolite genes (CCGs). We observed that ORE1 not only controls age-dependent (i.e. developmental) senescence, but also senescence induced by salinity: plants overexpressing ORE1 showed enhanced senescence under salt stress, while delayed senescence is observed in the ore1 mutant. We discovered that ORE1 interacts at the protein level with the Golden-like 2 TFs GLK1 and GLK2, both of which are required for chloroplast development and maintenance. Through this interaction, ORE1 inhibits the GLKs and thus lowers their capacity to maintain chloroplast function. Thus, ORE1, which is not expressed in young leaves but shows increased expression when leaves age, functions in a dual manner to control senescence, i.e. by activating SAGs and by inhibiting GLKs. We further discovered that the NAC TF ATAF1 binds to the promoters of GLK1 and ORE1. However, while ATAF1 rapidly represses the expression of GLK1, it activates the expression of ORE1, thereby shifting the leaf´s physiology towards senescence. Furthermore, ATAF1 induces a carbon starvation transcriptome and metabolome, in part through direct control of the TREHALASE1 (TRE1) gene, which encodes the only known trehalase in Arabidopsis. Notably, ATAF1 itself is induced in conditions that lead to carbon/energy starvation (e.g. drought, extended night, low CO2 concentration), indicating the presence of a positive feedback loop in which ATAF1 acts. Finally, we found that autophagy (ATG) genes are induced by ATAF1, consistent with the role of autophagy in protein recycling during developmental leaf senescence and adverse environmental conditions that trigger senescence. We also discovered, that a NAC TF whose expression rises relatively early during leaf senescence, extends plant longevity when overexpressed, which led us to name it JUNGBRUNNEN1 (JUB1). In addition, overexpression of JUB1 increases the plant´s tolerance to different abiotic stresses, including salinity and heat stress. JUB1 directly regulates key stress-related genes, including DREB2A. Furthermore, it dampens the cellular concentration of H2O2, which in part may explain the delay in senescence and the enhanced stress tolerance. In summary, the project funded within FOR948 has led to considerable progress of our understanding of the role of NAC transcription factors for transcriptional reprogramming during senescence and has established a solid basis for further research.

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