MtNF-YA1, a central transcriptional regulator of symbiotic nodule development, is also a determinant of medicago truncatula susceptibility toward a root pathogen

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Abstract

Plant NF-Y transcription factors control a wide array of biological functions enabling appropriate reproductive and developmental processes as well as adaptation to various abiotic and biotic environments. In Medicago truncatula, MtNF-YA1 was previously identified as a key determinant for nodule development and establishment of rhizobial symbiosis. Here, we highlight a new role for this protein in compatibility to Aphanomyces euteiches, a root pathogenic oomycete. The Mtnf-ya1-1 mutant plants showed better survival rate, reduced symptoms, and increased development of their root apparatus as compared to their wild-type (WT) background A17. MtNF-YA-1 was specifically up-regulated by A. euteiches in F83005.5, a highly susceptible natural accession of M. truncatula while transcript level remained stable in A17, which is partially resistant. The role of MtNF-YA1 in F83005.5 susceptibility was further documented by reducing MtNF-YA1 expression either by overexpression of the miR169q, a microRNA targeting MtNF-YA1, or by RNAi approaches leading to a strong enhancement in the resistance of this susceptible line. Comparative analysis of the transcriptome of WT and Mtnf-ya11 led to the identification of 1509 differentially expressed genes. Among those, almost 36 defense-related genes were constitutively expressed in Mtnf-ya1-1, while 20 genes linked to hormonal pathways were repressed. In summary, we revealed an unexpected dual role for this symbiotic transcription factor as a key player in the compatibility mechanisms to a pathogen.

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Rey, T., Laporte, P., Bonhomme, M., Jardinaud, M. F., Huguet, S., Balzergue, S., … Jacquet, C. (2016). MtNF-YA1, a central transcriptional regulator of symbiotic nodule development, is also a determinant of medicago truncatula susceptibility toward a root pathogen. Frontiers in Plant Science, 7(DECEMBER2016). https://doi.org/10.3389/fpls.2016.01837

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