Silicon induces metallochaperone-driven cadmium binding to the cell wall and restores redox status through elevated glutathione in Cd-stressed sugar beet.

Cadmium (Cd) is toxic; however, whether silicon (Si) alleviates Cd toxicity was never studied in sugar beet. The study was conducted on 2-week-old sugar beet cultivated in the presence or absence of Cd (10 µM CdSO4 ) and Si (1 mM Na2 SiO3 ) in hydroponic conditions. The morphological impairment and cellular damages observed in sugar beet upon Cd toxicity were entirely reversed due to Si. Si substantially restored the energy-providing ability, absorbed energy flux, and electron transport toward PSII, which might be correlated with the upregulation of BvIRT1 and ferric chelate reductase activity leading to the restoration of Fe status in Cd-stressed sugar beet. Although Si caused a reduction of shoot Cd, the root Cd substantially increased under Cd stress, a significant part of which was retained in the cell wall rather than in the root vacuole. While the concentration of phytochelatin and the expression of BvPCS3 (PHYTOCHELATIN SYNTHASE 3) showed no changes upon Si exposure, Si induced the expression of BvHIPP32 (HEAVY METAL-ASSOCIATED ISOPRENYLATED PLANT PROTEIN 32) in the Cd-exposed root. The BvHIPP32 and AtHIPP32 metallochaperone proteins are localized in the cell wall and they share similar sequence alignment, physiochemical properties, secondary structure, cellular localization, motif locations, domain association, and metal-binding site (cd00371) linked to the metallochaperone-like protein. It suggests that Si reduces the Cd level in shoot by retaining the excess Cd in the cell wall of roots due to the induction of BvHIPP32 gene. Also, Si stimulates glutathione-related antioxidants along with the BvGST23 expression, inferring an ascorbate-glutathione ROS detoxification pathway in Cd-exposed plants.

Arbuscular Mycorrhizal Symbiosis Mitigates Iron (Fe)-Deficiency Retardation in Alfalfa (Medicago sativa L.) Through the Enhancement of Fe Accumulation and Sulfur-Assisted Antioxidant Defense.

Iron (Fe)-deficiency is one of the major constraints affecting growth, yield and nutritional quality in plants. This study was performed to elucidate how arbuscular mycorrhizal fungi (AMF) alleviate Fe-deficiency retardation in alfalfa (Medicago sativa L.). AMF supplementation improved plant biomass, chlorophyll score, Fv/Fm (quantum efficiency of photosystem II), and Pi_ABS (photosynthesis performance index), and reduced cell death, electrolyte leakage, and hydrogen peroxide accumulation in alfalfa. Moreover, AMF enhanced ferric chelate reductase activity as well as Fe, Zn, S and P in alfalfa under Fe-deficiency. Although Fe-transporters (MsIRT1 and MsNramp1) did not induce in root but MsFRO1 significantly induced by AMF under Fe deficiency in roots, suggesting that AMF-mediated Fe enhancement is related to the bioavailability of Fe at rhizosphere/root apoplast rather than the upregulation of Fe transporters under Fe deficiency in alfalfa. Several S-transporters (MsSULTR1;1, MsSULTR1;2, MsSULTR1;3, and MsSULTR3;1) markedly increased following AMF supplementation with or without Fe-deficiency alfalfa. Our study further suggests that Fe uptake system is independently influenced by AMF regardless of the S status in alfalfa. However, the increase of S in alfalfa is correlated with the elevation of GR and S-metabolites (glutathione and cysteine) associated with antioxidant defense under Fe deficiency.

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.