Summary
Appropriate regulation of crop seed germination is of significance for agriculture production. In this study, we show that TaJAZ1, most closely related to Arabidopsis JAZ3, negatively modulates abscisic acid (ABA)‐inhibited seed germination and ABA‐responsive gene expression in bread wheat. Biochemical interaction assays demonstrate that the C‐terminal part containing the Jas domain of TaJAZ1 physically interacts with TaABI5.
Similarly, Arabidopsis jasmonate‐ZIM domain (JAZ) proteins also negatively modulate ABA responses. Further we find that a subset of JAZ proteins could interact with ABI5 using the luciferase complementation imaging assays.
Choosing JAZ3 as a representative, we demonstrate that JAZ3 interacts with ABI5 in vivo and represses the transcriptional activation activity of ABI5. ABA application could abolish the enrichment of JAZ proteins in the ABA‐responsive gene promoter. Furthermore, we find that ABA application could induce the expression of jasmonate (JA) biosynthetic genes and then increase the JA concentrations partially dependent on the function of ABI5, consequently leading to the degradation of JAZ proteins.
This study sheds new light on the crosstalk between JA and ABA in modulating seed germination in bread wheat and Arabidopsis.
Powdery mildew, caused by the biotrophic fungal pathogen
Blumeria graminis
f. sp.
tritici
, is a major limitation for wheat yield. However, the molecular mechanisms underlying wheat resistance against powdery mildew remain largely unclear. In this study, we report the role of JASMONATE-ZIM domain protein TaJAZ1 in regulating bread wheat resistance against powdery mildew. We generated transgenic bread wheat lines over-expressing the truncated TaJAZ1 without the Jas motif, which showed increased
TaPR1/2
gene expression and reactive oxygen species accumulation, leading to enhanced resistance against powdery mildew. Simultaneously, we identified a Jasmonic acid (JA)-induced bHLH transcription factor TaMYC4 in bread wheat. We demonstrated that TaJAZ1 directly interacts with TaMYC4 to repress its transcriptional activity. Meanwhile, we show that the ZIM domain of TaJAZ1 interacts with the C terminus of TaNINJA, whereas the N-terminal EAR motif of TaNINJA interacts with the transcriptional co-repressor TaTPL. Collectively, our work pinpoints
TaJAZ1
as a favorable gene to enhance bread wheat resistance toward powdery mildew, and provides a molecular framework for JA signaling in bread wheat.
The miR156-targeted SQUAMOSA PROMOTER BINDING PROTEIN-LIKE (SPL) transcription factors play key roles in regulating plant development, but little is known about their function in abscisic acid (ABA) signaling. Here, we report that the miR156-targeted SPLs enhance ABA responses and contribute to the inhibition of pre-harvest sprouting. We find that SPL9 directly activates the expression of ABA responsive genes through binding to their promoters. SPL9 was further shown to physically interact with ABSCISIC ACID INSENSITIVE 5 (ABI5), a master transcription factor in ABA signaling, thus promoting its association with the promoters of ABA responsive genes. Furthermore, we reveal that the protein kinases SnRK2s interact with and phosphorylate SPL9, which is essential for its role in the activation of ABA responses. Together, our results disclose a SnRK2s-SPLs-ABI5 regulatory module in ABA signaling in Arabidopsis.
The domestication gene Q is largely responsible for the widespread cultivation of wheat because it confers multiple domestication traits. However, the underlying molecular mechanisms of how Q regulates these domestication traits remain unclear. In this study, we identify a Q-interacting protein TaLAX1, a basic helix-loop-helix transcription factor, through yeast two-hybrid assays. Using biochemical and genetic approaches, we explore the roles of TaLAX1 in regulating wheat domestication traits. Overexpression of TaLAX1 produces phenotypes, reminiscent of the q allele; loss-of-function Talax1 mutations confer compact spikes, largely similar to the Q-overexpression wheat lines. The two transcription factors TaLAX1 and Q disturb each other's activity to antagonistically regulate the expression of the lignin biosynthesis-related gene TaKNAT7-4D. More interestingly, a natural variation (InDel, +/À TATA), which occurs in the promoter of TaLAX1, is associated with the promoter activity difference between the D subgenome of bread wheat and its ancestor Aegilops tauschii accession T093. This study reveals that the transcription factor TaLAX1 physically interacts with Q to antagonistically regulate wheat domestication traits and a natural variation (InDel, +/À TATA) is associated with the diversification of TaLAX1 promoter activity.
CONSTANS (CO) is a central regulator of floral initiation in response to photoperiod. In this study, we show that the GSK3 kinase BIN2 physically interacts with CO and the gain-of-function mutant bin2-1 displays late flowering phenotype through down-regulation of FT transcription. Genetic analyses show that BIN2 genetically acts upstream of CO in regulating flowering time. Further, we illustrate that BIN2 phosphorylates the Thr280 residue of CO. Importantly, the BIN2 phosphorylation of Thr280 residue restricts the function of CO in promoting flowering through affecting its DNA-binding activity. Moreover, we reveal that the N-terminal part of CO harboring the B-Box domain mediates the interaction of both CO-CO and BIN2-CO. We find that BIN2 inhibits the formation of CO dimer/oligomer. Taken together, this study reveals that BIN2 regulates flowering time through phosphorylating the Thr280 of CO and inhibiting the CO-CO interaction in Arabidopsis.
CONSTANS (CO) is a central regulator of floral initiation in response to photoperiod. In this study, we show that the GSK3 kinase BIN2 physically interacts with CO and the gain-of-function mutant bin2-1 displays late flowering phenotype through down-regulation of FT transcription. Genetic analyses show that BIN2 genetically acts upstream of CO in regulating flowering time. Further, we illustrate that BIN2 phosphorylates the Thr280 residue of CO. Importantly, the BIN2 phosphorylation of Thr280 residue restricts the function of CO in promoting flowering. Moreover, we reveal that the N-terminal part of CO harboring the B-Box domain mediates the interaction of both CO-CO and BIN2-CO. We find that BIN2 inhibits the formation of CO dimer/oligomer. Taken together, this study reveals that BIN2 regulates flowering time through phosphorylating the Thr280 of CO and inhibiting the CO-CO interaction in Arabidopsis.HighlightBIN2 regulates flowering time through phosphorylating the Thr280 of CO in Arabidopsis.
Summary
Drought stress causes substantial losses in crop production per year worldwide, threatening global food security. Identification of the genetic components underlying drought tolerance in plants is of great importance. In this study, we report that loss‐of‐function of the chromatin‐remodeling factor PICKLE (PKL), which is involved in repression of transcription, enhances drought tolerance of Arabidopsis.
At first, we find that PKL interacts with ABI5 to regulate seed germination, but PKL regulates drought tolerance independently of ABI5. Then, we find that PKL is necessary for repressing the drought‐tolerant gene AFL1, which is responsible for the drought‐tolerant phenotype of pkl mutant. Genetic complementation tests demonstrate that the Chromo domain and ATPase domain but not the PHD domain are required for the function of PKL in regulating drought tolerance. Interestingly, we find that the DNA‐binding domain (DBD) is essential for the protein stability of PKL.
Furthermore, we demonstrate that the SUMO E3 ligase MMS21 interacts with and enhances the protein stability of PKL. Genetic interaction analysis shows that MMS21 and PKL additively regulate plant drought tolerance.
Collectively, our findings uncover a MMS21‐PKL‐AFL1 module in regulating plant drought tolerance and offer insights into a novel strategy to improve crop drought tolerance.
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