Repression of Nitrogen Starvation Responses by Members of the Arabidopsis GARP-Type Transcription Factor NIGT1/HRS1 Subfamily
Author(s) -
Takatoshi Kiba,
Jun Inaba,
Toru Kudo,
Nanae Ueda,
Mineko Konishi,
Nobutaka Mitsuda,
Yuko Takiguchi,
Youichi Kondou,
Takeshi Yoshizumi,
Masaru OhmeTakagi,
Minami Matsui,
Kentaro Yano,
Shuichi Yanagisawa,
Hitoshi Sakakibara
Publication year - 2018
Publication title -
the plant cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.324
H-Index - 341
eISSN - 1532-298X
pISSN - 1040-4651
DOI - 10.1105/tpc.17.00810
Subject(s) - biology , transcription factor , psychological repression , arabidopsis , gene , transcriptome , arabidopsis thaliana , genetics , subfamily , microbiology and biotechnology , gene expression , regulation of gene expression , promoter , transcription (linguistics) , mutant , linguistics , philosophy
Nitrogen (N) is often a limiting nutrient whose availability determines plant growth and productivity. Because its availability is often low and/or not uniform over time and space in nature, plants respond to variations in N availability by altering uptake and recycling mechanisms, but the molecular mechanisms underlying how these responses are regulated are poorly understood. Here, we show that a group of GARP G2-like transcription factors, Arabidopsis thaliana NITRATE-INDUCIBLE, GARP-TYPE TRANSCRIPTIONAL REPRESSOR1/HYPERSENSITIVE TO LOW Pi-ELICITED PRIMARY ROOT SHORTENING1 proteins (NIGT1/HRS1s), are factors that bind to the promoter of the N starvation marker NRT2.4 and repress an array of N starvation-responsive genes under conditions of high N availability. Transient assays and expression analysis demonstrated that NIGT1/HRS1s are transcriptional repressors whose expression is regulated by N availability. We identified target genes of the NIGT1/HRS1s by genome-wide transcriptome analyses and found that they are significantly enriched in N starvation response-related genes, including N acquisition, recycling, remobilization, and signaling genes. Loss of NIGT1/HRS1s resulted in deregulation of N acquisition and accumulation. We propose that NIGT1/HRS1s are major regulators of N starvation responses that play an important role in optimizing N acquisition and utilization under fluctuating N conditions.
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