Phosphorus (P) is a macronutrient necessary for plant growth and development. Inorganic phosphate (Pi) deficiency modulates the signaling pathway of the phytohormone jasmonate in Arabidopsis thaliana, but the underlying molecular mechanism currently remains elusive. Here, we confirmed that jasmonate signaling was enhanced under low Pi conditions, and the CORONATINE INSENSITIVE1 (COI1)-mediated pathway is critical for this process. A mechanistic investigation revealed that several JASMONATE ZIM-DOMAIN (JAZ) repressors physically interacted with the Pi signaling-related core transcription factors PHOSPHATE STARVATION RESPONSE1 (PHR1), PHR1-LIKE2 (PHL2), and PHL3. Phenotypic analyses showed that PHR1 and its homologs positively regulated jasmonate-induced anthocyanin accumulation and root growth inhibition. PHR1 stimulated the expression of several jasmonate-responsive genes, whereas JAZ proteins interfered with its transcriptional function. Furthermore, PHR1 physically associated with the basic helix-loop-helix (bHLH) transcription factors MYC2, MYC3, and MYC4. Genetic analyses and biochemical assays indicated that PHR1 and MYC2 synergistically increased the transcription of downstream jasmonate-responsive genes and enhanced the responses to jasmonate. Collectively, our study reveals the crucial regulatory roles of PHR1 in modulating jasmonate responses, and provides a mechanistic understanding of how PHR1 functions together with JAZ and MYC2 to maintain the appropriate level of jasmonate signaling under conditions of Pi deficiency.
The phytohormone jasmonate is an essential endogenous signal to regulate multiple plant processes for environmental adaptations, such as primary root growth inhibition and root hair elongation. Perception of environmental stresses promotes the accumulation of jasmonate which is sensed by the CORONATINE INSENSITIVE1 (COI1)-JASMONATE ZIM-DOMAIN (JAZ) co-receptor, triggering the degradation of JAZ repressors and induction of transcriptional reprogramming. The basic helix-loop-helix (bHLH) subgroup IIIe transcription factors MYC2, MYC3, and MYC4 are the most extensively characterized JAZ-binding factors and together stimulate jasmonate-signaled primary root growth inhibition. Conversely, the bHLH subgroup IIId transcription factors (i.e. bHLH3 and bHLH17) physically associate with JAZ proteins and suppress jasmonate-induced root growth inhibition. For root hair development, JAZ proteins interact with and inhibit ROOT HAIR DEFECTIVE 6 (RHD6) and RHD6 LIKE1 (RSL1) transcription factors to modulate jasmonate-enhanced root hair elongation. Moreover, jasmonate also interacts with other signaling pathways (such as ethylene and auxin) to regulate primary root growth and/or root hair elongation. Here, we review the recent progresses that have provided insights into jasmonate-mediated primary root growth and root hair development.
CONSTANS (CO) is a critical regulator of flowering that combines photoperiodic and circadian signals in Arabidopsis (Arabidopsis thaliana). CO is expressed in multiple tissues, including seedling roots and young leaves. However, the roles and underlying mechanisms of CO in modulating physiological processes outside of flowering remain obscure. Here, we show that the expression of CO responds to salinity treatment. CO negatively mediated salinity tolerance under long-day (LD) conditions. Seedlings from co mutants were more tolerant to salinity stress, whereas overexpression of CO resulted in plants with reduced tolerance to salinity stress. Further genetic analyses revealed the negative involvement of GIGANTEA (GI) in salinity tolerance requires a functional CO. Mechanistic analysis demonstrated that CO physically interacts with four critical basic leucine zipper (bZIP) transcription factors; ABSCISIC ACID-RESPONSIVE ELEMENT BINDING FACTOR1 (ABF1), ABF2, ABF3, and ABF4. Disrupting these ABFs made plants hypersensitive to salinity stress, demonstrating that ABFs enhance salinity tolerance. Moreover, ABF mutations largely rescued the salinity-tolerant phenotype of co mutants. CO suppresses the expression of several salinity-responsive genes and influences the transcriptional regulation function of ABF3. Collectively, our results show that the LD-induced CO works antagonistically with ABFs to modulate salinity responses, thus revealing how CO negatively regulates plant adaptation to salinity stress.
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