Iron deficiency in plants: an update on homeostasis and its regulation by nitric oxide and phytohormones

Coping with salt stress-interaction of halotolerant bacteria in crop plants: A mini review

“…Another major challenge for salinity-stressed crops is the low availability of soluble ferrous ions (Fe 2+ ) (iron form uptake by plants), which is determined primarily by the soil pH (available at acidic pH 6). Saline soils have alkaline pH (pH > 6.5) that causes the oxidation of ferrous ion (Fe 2+ ) to ferric ion (Fe 3+ ) and reduces the availability of iron to plants (Mahawar et al, 2022 ). The production of siderophores by HT-PGPR chelates Fe 3+ and compensates the iron (Fe) requirement in salt-stressed crops (Kumar Arora et al, 2020 ).…”

NO Is Not the Same as GSNO in the Regulation of Fe Deficiency Responses by Dicot Plants

“…In the 1980s, NO was recognized as a signaling molecule in mammals and later on, around the 1990s, also in plants [ 19 , 21 ]. NO has been involved in a myriad of developmental and physiological processes of plants, including seed germination, stomatal closure, flower development, root branching and senescence [ 20 , 22 , 23 , 24 , 25 ]. In addition, NO has been implicated in the responses of plants to both biotic and abiotic stresses, including pathogen infection, salinity, drought stress, nutrient deficiencies, an excess of heavy metals and others (see Section 3 ; Refs.…”

“…NO synthesis has been reported in different plant organs, including roots, stems, leaves and flowers, and, at the subcellular level, both in the apoplast and in the symplast, and in different organelles, such as mitochondria, chloroplasts and peroxisomes [ 20 , 33 ]. NO can be synthesized by both enzymatic and non-enzymatic pathways [ 19 , 20 , 22 , 24 , 33 ]. In mammals, NO synthases (NOS) catalyze the conversion of L-arginine to NO and citrulline.…”

“…These authors showed that NO production was enhanced in Fe-deficient tomato roots; that the NO-scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) blocked the enhanced ferric reductase activity and the expression of several key Fe acquisition genes, including FER , FRO1 and IRT1 , in Fe-deficient tomato roots; that the NO donor GSNO induced the development of subapical root hairs and the expression of several Fe acquisition genes in roots of tomato plants grown under low Fe conditions; and that NO-deficient mutants, such as the NR-deficient tomato nia mutants, were impaired in the activation of Fe deficiency responses [ 34 ]. After that, similar results have been found by other authors in different dicot plant species by determining NO in roots; by using NO scavengers (e.g., cPTIO), NR inhibitors (e.g., tungstate) or NOS inhibitors (e.g., L-NAME); by using NO donors (e.g., sodium nitroprusside, diethylamine-NONOate or GSNO); and by using NO-defective mutants [ 7 , 10 , 11 , 13 , 15 , 16 , 20 , 24 , 66 , 71 , 76 , 96 , 97 , 98 , 99 , 100 , 101 , 102 ]. It should be noted that sodium nitroprusside is not an adequate NO donor for Fe studies since it contains an Fe atom [ 20 ].…”

“…NO can interact with many hormones, such as strigolactones, salicylic acid, abscisic acid, auxin and ethylene, and signaling molecules, such as polyamines, reactive oxygen species and hydrogen sulfide, to exert its functions in the regulation of responses to biotic and abiotic stresses [ 18 , 29 , 33 , 55 , 71 , 119 , 120 , 121 , 122 , 123 , 124 ]. In the regulation of Fe deficiency responses by dicot plants, some of these interactions have already been described [ 8 , 9 , 24 , 71 , 105 ]. Nonetheless, to simplify the description of all the possible interactions, in this review, we will only describe the interactions of NO with ethylene and auxin.…”