Signaling pathways that control the activities in non-photosynthetic plastids, important sites of plant metabolism, are largely unknown. Previously, we demonstrated that WRKY2 and WRKY34 transcription factors play an essential role in pollen development downstream of mitogen-activated protein kinase 3 (MPK3) and MPK6 in Arabidopsis. Here, we report that GLUCOSE-6-PHOSPHATE/PHOSPHATE TRANSLOCATOR 1 (GPT1) is a key target gene of WRKY2/WRKY34. GPT1 transports glucose-6-phosphate (Glc6P) into plastids for starch and/or fatty acid biosynthesis depending on the plant species. Loss of function of WRKY2/WRKY34 results in reduced GPT1 expression, and concomitantly, reduced accumulation of lipid bodies in mature pollen, which leads to compromised pollen viability, germination, pollen tube growth, and male transmission in Arabidopsis. Pollen-specific overexpression of GPT1 rescues the pollen defects of wrky2 wrky34 double mutant. Furthermore, gain-of-function activation of MPK3/MPK6 enhances GPT1 expression; whereas GPT1 expression is reduced in mkk4 mkk5 double mutant. Together, this study revealed a cytoplasmic/nuclear signaling pathway capable of coordinating the metabolic activities in plastids. High-level expression of GPT1 at late stages of pollen development drives Glc6P from cytosol into plastids, where Glc6P is used for fatty acid biosynthesis, an important step of lipid body biogenesis. The accumulation of lipid bodies during pollen maturation is essential to pollen fitness and successful reproduction.

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Plant growth and development rely on sugar transport between source and sink cells and between different organelles. The plastid-localized sugar transporter GLUCOSE-6-PHOSPHATE TRANSLOCATER1 (GPT1) is an essential gene in Arabidopsis (Arabidopsis thaliana). Using a partially rescued gpt1 mutant and cell-specific RNAi suppression of GPT1, we demonstrated that GPT1 is essential to the function of the embryo suspensor and the development of the embryo. GPT1 showed a dynamic expression/accumulation pattern during embryogenesis. Inhibition of GPT1 accumulation via RNAi using a suspensor-specific promoter resulted in embryos and seedlings with defects similar to auxin mutants. Loss of function of GPT1 in the suspensor also led to abnormal/ectopic cell division in the lower part of the suspensor, which gave rise to an ectopic embryo, resulting in twin embryos in some seeds. Furthermore, loss of function of GPT1 resulted in vacuolar localization of PIN-FORMED1 (PIN1) and altered DR5 auxin activity. Proper localization of PIN1 on the plasma membrane is essential to polar auxin transport and distribution, a key determinant of pattern formation during embryogenesis. Our findings suggest that the function of GPT1 in the embryo suspensor is linked to sugar and/or hormone distribution between the embryo proper and the maternal tissues, and is important for maintenance of suspensor identity and function during embryogenesis.

Despite the importance of lipid metabolism in various biological processes, little is known about the functionality of ATS1, a plastid glycerol-3-phosphate acyltransferase catalyzing the initial step of the prokaryotic glycerolipids biosynthetic pathway, in plant response to salt stress. In this study, both the loss-of-function mutants and the overexpression lines of ATS1 were analyzed for salt tolerance properties. The results showed that ATS1 overexpression lines had lower seed germination, shoot biomass, chlorophyll content, the proportion of relatively normal pod, and higher root/shoot ratio and anthocyanidin content compared with the wild type. Physiological and biochemical analysis revealed that ats1 mutants had more unsaturated fatty acids to stabilize the plasma membrane under salt damage. Additionally, less induction of three main antioxidant enzymes activity and lower MDA content in ats1 mutants indicated that mutation of the ATS1 gene could reduce the damage extent. Furthermore, the ats1 mutants maintained the K+/Na+ homeostasis by upregulating HAK5 expression to increase K+ absorption and down-regulating HKT1 expression to prevent Na+ uptake. This study suggested that the ATS1 gene negatively affects salt resistance in Arabidopsis.