PHOSPHATE STARVATION RESPONSE1 (PHR1) interacts with JASMONATE ZIM-DOMAIN (JAZ) and MYC2 to modulate phosphate deficiency-induced jasmonate signaling in Arabidopsis.

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.

CONSTANS interacts with and antagonizes ABF transcription factors during salt stress under long-day conditions.

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 4 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.

Jasmonate-regulated root growth inhibition and root hair elongation.

The phytohormone jasmonate is an essential endogenous signal in the regulation of multiple plant processes for environmental adaptation, 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 recent progress into jasmonate-mediated primary root growth and root hair development.

Molecular mechanism of phosphorous signaling inducing anthocyanin accumulation in Arabidopsis.

Anthocyanins, flavonoid compounds derived from secondary metabolic pathways, play important roles in various biological processes. Phosphorus (P) is an essential macroelement for plant growth and development, and P-starvation usually results in anthocyanin accumulation. However, the molecular mechanism of P deficiency promotes anthocyanin biosynthesis has not been well characterized. Here, we provided evidence that the P signaling core protein PHOSPHATE STARVATION RESPONSE1 (PHR1) is physically associate with transcription factors (TFs) involved in anthocyanidin biosynthesis, including PRODUCTION OF ANTHOCYANIN PIGMENTS1 (PAP1/MYB75), MYB DOMAIN PROTEIN 113 (MYB113) and TRANSPARENT TESTA 8 (TT8). PHR1 and its homologies positively regulated anthocyanin accumulation in Arabidopsis seedlings under P-deficient conditions. Disruption of PHR1 simultaneously rendered seedlings hyposensitive to limiting P, whereas the overexpression of PHR1 enhanced P- deficiency-induced anthocyanin accumulation. Genetic analysis demonstrated that 35S:PHR1-2HA-5 seedlings partially recovers the P deficiency insensitive phenotype of myb-RNAi and tt8 mutants. In summary, our study indicated that protein complexes formed by PHR1 and MBW complex directly mediate the process of P-deficiency-induced anthocyanin accumulation, providing a new mechanistic understanding of how P-deficient signaling depends on the endogenous anthocyanin synthesis pathway to promote anthocyanin accumulation in Arabidopsis.

[Artesunate in interrupting the transmission of Plasmodium falciparum].

OBJECTIVE: To observe the effect of artesunate (ATS) on the infectivity of Plasmodium falciparum gametocytes (PFG). METHODS: 31 volunteers with falciparum malaria and gametocytaemia were randomly divided into 3 groups: artesunate (ATS) group (15 cases), quinine (QN) group (10 cases) and placebo group (6 cases). Each case in ATS group received 6-day course of oral artesunate (200 mg at 0, 6 and 24 hours then 100 mg daily for 4 days). Cases in QN group each received 21-dose course of quinine sulfate (500 mg/time) over seven days. Cases in placebo group took 2 tablets of vitamin B composites, three times per day for seven days. Peripheral PFG were counted daily in all cases until the clearance of PFG. Mosquitoes (Anopheles dirus) were fed with venous blood of patients on the 1st, 7th, 14th, 21st and 28th day, respectively. RESULTS: All cases in placebo group were PFG positive at the whole course by blood smear examinations. The PFG relative density in ATS group were (12.5+/-3.3)%, (1.2+/-0.4)%, (0.3+/-0.1)% on 7th, 14th, 21st day respectively, and the mean PFG clearance time was (22.0+/-1.4) d. The PFG relative density in QN group were (173.9+/-47.0)%, (112.5+/-45.4)%, (32.5+/-17.8)% at 7th, 14th, 21st day respectively, and the mean clearance time of PFG was (32.5+/-2.1) d (t=4.731, P<0.01). PFG remained positive on the 28th day in placebo group. The infectivity test to mosquitoes showed on 14th day the positive rate in ATS group, QN group and placebo group were 0, 35.0% and 48.7% respectively. In ATS group, the sporozoite rate of anopheline mosquitoes were 14.8% and 0 at 7th, 14th day, while in QN group, 142.0%, 98.6% and 20.3% at 7th, 14th, 21st day respectively. In placebo group, the infection rate of sporozoites remained stable. CONCLUSION: Oral administration of artesunate with a total dosage of 1000 mg in 6 days inhibits the infectivity of PFG.