GIGANTEA regulates PAD4 transcription to promote pathogen defense against Hyaloperonospora arabidopsidis in Arabidopsis thaliana

ABSTRACT

Plants have evolved a network of complex signaling pathways that allow them to cope with the fluctuations of internal and external environmental cues. GIGANTEA (GI), a well-known, highly conserved plant nuclear protein, has been shown to regulate multiple biological functions in plants such as circadian rhythm, light signaling, cold tolerance, hormone signaling, and photoperiodic flowering. Recently, the role of GI in disease tolerance against different pathogens has come to light; however, a detailed mechanism to understand the role of GI in pathogen defense remains largely unexplained. Here, we report that GIGANTEA is upregulated upon infection with a virulent oomycete pathogen, Hyaloperonospora arabidopsidis (Hpa), in Arabidopsis thaliana accession Col-0. To investigate the role of GI in Arabidopsis defense, we examined the pathogen infection phenotype of gi mutant plants and found that gi-100 mutant was highly susceptible to Hpa Noco2 infection. Notably, the quantitative real-time PCR showed that PHYTOALEXIN DEFICIENT4 (PAD4) and several PAD4-regulated downstream genes were downregulated upon Noco2 infection in gi-100 mutant as compared to Col-0 plants. Furthermore, the chromatin immunoprecipitation results show that GI can directly bind to the intronic region of the PAD4 gene, which might explain the mechanism of GI function in regulating disease resistance in plants. Taken together, our results suggest that GI expression is induced upon Hpa pathogen infection and GI can regulate the expression of PAD4 to promote resistance against the oomycete pathogen Hyaloperonospora arabidopsidis in Arabidopsis thaliana.

KEYWORDS:

• GIGANTEA
• plant defense response
• Hyaloperonospora
• PAD4
• salicylic acid (SA)
• basal immunity

Acknowledgments

We thank Dr Jane Parker for providing Ws-2 and eds1-2 mutant seeds and for her helpful discussions during the whole project. We also thank Prof. George Coupland, Max Planck Institute, for providing Col-0, 35S::HA:GI, gi-2 and gi-100 mutant seeds. Special thanks to Jaqueline Bautor for her guidance in performing pathogen experiments. A big thanks to Dr Ankita Singh, Dr Aparajita Singh and Dr Kishore Panigrahi for proofreading the manuscript.

Author contributions

AS has designed and performed the experiments. AS has analyzed the data, written the manuscript and arranged the figures.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Supplementary material

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Additional information

Funding

This work was supported by the Max-Planck Institute for Plant Breeding Research, Carl-von-Linne-Weg 10, 50829, Cologne, Germany; Department of Science and Technology, Science Engineering Research Board, India (Grant No. EMR/2014/000533); and Department of Atomic Energy, National Institute of Science Education and Research, India. We also acknowledge CSIR and DAAD-PhD exchange program for providing the funds.