Abstract
The function of miR165/166 in plant growth and development has been extensively studied, however, its roles in abiotic stress responses remain largely unknown. Here, we report that reduction in the expression of miR165/166 conferred a drought and cold resistance phenotype and hypersensitivity to ABA during seed germination and post-germination seedling development. We further show that the ABA hypersensitive phenotype is associated with a changed transcript abundance of ABA-responsive genes and a higher expression level of ABI4, which can be directly regulated by a miR165/166 target. Additionally, we found that reduction in miR165/166 expression leads to elevated ABA levels, which occurs at least partially through the increased expression of BG1, a gene that is directly regulated by a miR165/166 target. Taken together, our results uncover a novel role for miR165/166 in the regulation of ABA and abiotic stress responses and control of ABA homeostasis.
Highlights
The phytohormone abscisic acid (ABA) plays critical roles in plant growth and development, such as seed maturation, seed germination, seedling growth, stomatal movement, as well as plant responses to abiotic and biotic stress, including drought, salinity, cold and pathogen infection [1,2,3,4]
Little is known about how a miRNA may perform critical functions in both plant development and abiotic stress responses
One well-known miRNA, miR165/ 166, has critical roles in plant development. We show that this miRNA has important functions in ABA and abiotic stress responses
Summary
The phytohormone abscisic acid (ABA) plays critical roles in plant growth and development, such as seed maturation, seed germination, seedling growth, stomatal movement, as well as plant responses to abiotic and biotic stress, including drought, salinity, cold and pathogen infection [1,2,3,4]. The fluctuation of cellular ABA levels, which are determined by biosynthetic and catabolic pathways, allow plants to cope with physiological and environmental conditions [5,6,7]. An additional biosynthetic pathway occurs through hydrolysis of Glc-conjugated ABA (abscisic acid-glucose ester [ABA-GE]) to ABA by two glucosidases, AtBG1 and AtBG2, which localize to the ER and vacuole, respectively [10, 11]. Hydroxylation and conjugation are catabolic pathways that mediate the fine-tuning of ABA levels. Members of the cytochrome P450 family, CYP707A1 to CYP707A4, control the hydroxylation reaction, and ABA uridine diphosphate glucosyltransferase (UGT) catalyzes the conjugation of ABA with Glc to produce ABA-GE [12,13,14,15,16,17]
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