Role of plastids and mitochondria in the early development of seedlings in dark growth conditions.

Establishment of the seedlings is a crucial stage of the plant life cycle. The success of this process is essential for the growth of the mature plant. In Nature, when seeds germinate under the soil, seedlings follow a dark-specific program called skotomorphogenesis, which is characterized by small, non-green cotyledons, long hypocotyl, and an apical hook-protecting meristematic cells. These developmental structures are required for the seedlings to emerge quickly and safely through the soil and gain autotrophy before the complete depletion of seed resources. Due to the lack of photosynthesis during this period, the seed nutrient stocks are the primary energy source for seedling development. The energy is provided by the bioenergetic organelles, mitochondria, and etioplast (plastid in the dark), to the cell in the form of ATP through mitochondrial respiration and etio-respiration processes, respectively. Recent studies suggest that the limitation of the plastidial or mitochondrial gene expression induces a drastic reprogramming of the seedling morphology in the dark. Here, we discuss the dark signaling mechanisms involved during a regular skotomorphogenesis and how the dysfunction of the bioenergetic organelles is perceived by the nucleus leading to developmental changes. We also describe the probable involvement of several plastid retrograde pathways and the interconnection between plastid and mitochondria during seedling development. Understanding the integration mechanisms of organellar signals in the developmental program of seedlings can be utilized in the future for better emergence of crops through the soil.

Tormentic acid, a triterpenoid isolated from the fruits of Chaenomeles speciose, protected indomethacin-induced gastric mucosal lesion via modulating miR-139 and the CXCR4/CXCL12/PLC/PKC/Rho a/MLC pathway.

CONTEXT: Tormentic acid (TA), an effective triterpenoid isolated from Chaenomeles speciosa (Sweet) Nakai (Rosaceae) fruits, exerts an effective treatment for gastric damage. OBJECTIVE: To investigate the gastroprotective effect of TA on indomethacin (IND) damaged GES-1 cells and rats, and explore potential mechanisms. MATERIALS AND METHODS: TA concentrations of 1.563-25 µM were used. Cell proliferation, apoptosis and migration were performed using MTT, colony formation, wound healing, migration, Hoechst staining assays. SD rats were divided into control, IND, TA (1, 2 and 4 mg/kg) + IND groups, once a day for 21 continuous days. Twenty-four hours after the last administration, all groups except the control group were given IND (100 mg/kg) by gavage. Gastric juice parameters, gastric ulcer, gastric blood flow (GBF), blood biochemical parameters and cytokine analysis and gastric mucosal histopathology were detected for 2 h and 6 h after IND oral administration. The mRNA and protein expression of miR-139 and the CXCR4/CXCL12/PLC/PKC/Rho A/MLC pathway were analyzed in the IND-damaged GES-1 cells and gastric tissue of rats. RESULTS: TA might ameliorate the gastric mucosal injury by accelerating the IND-damaged GES-1 cell proliferation and migration, ameliorating GBF, ulcer area and pathologic changes, the redox system and cytokine levels, the gastric juice parameters, elevating the gastric pH in IND damaged rats; suppressed miR-139 mRNA expression, elevated CXCR4 and CXCL12 mRNA and protein expression, p-PLC, p-PKC, Rho A, MLCK and p-MLC protein expression. DISCUSSION AND CONCLUSIONS: TA may have potential use as a clinical drug candidate for gastric mucosal lesion treatment.

Early-stage iron deficiency alters physiological processes and iron transporter expression, along with photosynthetic and oxidative damage to sorghum.

Iron (Fe) starvation in Strategy II plants is a major nutritional problem causing severe visual symptoms and yield reductions. This prompted us to investigate the physiological and molecular consequences of Fe deficiency responses at an early stage in sorghum plants. The Fe-starved sorghum did not show shoot biomass reduction, but the root length, biomass, and chlorophyll synthesis were severely affected. The chlorophyll a fluorescence analysis showed that the quantum yield efficiency of PSII (Fv/Fm) and photosynthesis performance index (Pi_ABS) in young leaves significantly reduced in response to low Fe. Besides, Fe concentration in root and shoot significantly declined in Fe-starved plants relative to Fe-sufficient plants. Accordingly, this Fe reduction in tissues was accompanied by a marked decrease in PS-release in roots. The qPCR experiment showed the downregulation of SbDMAS2 (deoxymugineic acid synthase 2), SbNAS3 (nicotianamine synthase 3), and SbYSL1 (Fe-phytosiderophore transporter yellow stripe 1) in Fe-deprived roots, suggesting that decreased rhizosphere mobilization of Fe(III)-PS contributes to reduced uptake and long-distance transport of Fe. The cis-acting elements of these gene promoters are commonly responsive to abscisic acid and methyl jasmonate, while SbYSL1 additionally responsive to salicylic acid. Further, antioxidant defense either through metabolites or antioxidant enzymes is not efficient in counteracting oxidative damage in Fe-deprived sorghum. These findings may be beneficial for the improvement of sorghum genotypes sensitive to Fe-deficiency through breeding or transgenic approaches.

Arbuscular mycorrhizal fungi mitigate Fe deficiency symptoms in sorghum through phytosiderophore-mediated Fe mobilization and restoration of redox status.

Sustainable management of iron (Fe) deficiency through the microbial association is highly desirable to ensure crop yield. This study elucidates whether and how arbuscular mycorrhizal fungi (AMF) ameliorate Fe deficiency symptoms in sorghum. AMF inoculation showed a significant improvement in plant biomass, chlorophyll score, Fv/Fm (quantum efficiency of photosystem II), and Pi_ABS (photosynthesis performance index), suggesting its potentiality to diminish Fe deficiency symptoms in sorghum. This AMF-driven prevention of Fe deficiency was further supported by the improvement of biochemical stress indicators, such as cell death, electrolyte leakage, hydrogen peroxide, and superoxide anion. In this study, AMF showed a significant increase in phytosiderophore (PS) release as well as Fe and S concentrations in sorghum under Fe deficiency. Quantitative real-time PCR analysis demonstrated the consistent upregulation of SbDMAS2 (deoxymugineic acid synthase 2), SbNAS2 (nicotianamine synthase 2), and SbYS1 (Fe-phytosiderophore transporter yellow stripe) in roots due to AMF with Fe deficiency. It suggests that the enhancement of Fe due to AMF is related to the mobilization of Fe(III)-PS in the rhizosphere supported by the long-distance transport of Fe by SbYS1 transporter in sorghum. Our study further showed that the elevation of S mainly in the presence of AMF possibly enhances the S-containing antioxidant metabolites (Met, Cys, and GSH) as well as enzymes (CAT, SOD, and GR) to counteract H2O2 and O2- for the restoration of redox status in Fe-deprived sorghum. Moreover, S possibly participates in Strategy II responses revealing its crucial role as a signaling molecule for Fe homeostasis in sorghum.

Arbuscular mycorrhizal fungi alleviate Fe-deficiency symptoms in sunflower by increasing iron uptake and its availability along with antioxidant defense.

Iron (Fe)-deficiency causes chlorosis and growth inhibition in sunflower, an important commercial crop. This study examines whether and how arbuscular mycorrhizal fungi (AMF) ameliorate Fe-deficiency symptoms in Fe-deficiency sensitive sunflower plants. AMF supplementation showed a significant improvement in plant biomass, chlorophyll score, Fv/Fm (quantum efficiency of photosystem II), and Pi_ABS (photosynthesis performance index), suggesting its beneficial effect under Fe deficiency. This AM-driven amelioration of Fe deficiency was further supported by the improvement of biochemical stress indicators, such as cell death, electrolyte leakage, superoxide anion, and hydrogen peroxide. In this study, the AMF supplementations resulted in significant improvement in Fe as well as Zn concentrations in root and shoot of sunflower under Fe deficiency. One of the primary Strategy-I responses, ferric reductase activity along with the expression of its respective gene (HaFRO1), significantly increased in roots due to AMF ensuring Fe availability in the rhizosphere under Fe deficiency. Our qPCR analysis also showed a significant upregulation of HaIRT1, HaNramp1, and HaZIP1 in roots of sunflower in the presence of AMF, suggesting that Fe and Zn transporters are concurrently involved with AMF-mediated alleviation of Fe deficiency. Further, AMF accelerates the activities of CAT and SOD, predominantly in roots to protect sunflower plants from Fe-deficiency reactive oxygen species (ROS). This study unveils the mechanistic basis of AMF to limit Fe deficiency retardation in sunflower.