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Serotonin (5-HT), an indoleamine compound, has been known to mediate many physiological responses of plants under environmental stress. The deep-seeding (≥20 cm) of maize seeds is an important cultivation strategy to ensure seedling emergence and survival under drought stress. However, the role of 5-HT in maize deep-seeding tolerance remains unexplored. Understanding the mechanisms and evaluating the optimal concentration of 5-HT in alleviating deep-seeding stress could benefit maize production. In this study, two maize inbred lines were treated with or without 5-HT at both sowing depths of 20 cm and 3 cm, respectively. The effects of different concentrations of 5-HT on the growth phenotypes, physiological metabolism, and gene expression of two maize inbred lines were examined at the sowing depths of 20 cm and 3 cm. Compared to the normal seedling depth of 3 cm, the elongation of the mesocotyl (average elongation 3.70 cm) and coleoptile (average elongation 0.58 cm), secretion of indole-3-acetic acid (IAA; average increased 3.73 and 0.63 ng g−1 FW), and hydrogen peroxide (H2O2; average increased 1.95 and 0.63 μM g−1 FW) in the mesocotyl and coleoptile were increased under 20 cm stress, with a concomitant decrease in lignin synthesis (average decreased 0.48 and 0.53 A280 g−1). Under 20 cm deep-seeding stress, the addition of 5-HT activated the expression of multiple genes of IAA biosynthesis and signal transduction, including Zm00001d049601, Zm00001d039346, Zm00001d026530, and Zm00001d049659, and it also stimulated IAA production in both the mesocotyl and coleoptile of maize seedlings. On the contrary, 5-HT suppressed the expression of genes for lignin biosynthesis (Zm00001d016471, Zm00001d005998, Zm00001d032152, and Zm00001d053554) and retarded the accumulation of H2O2 and lignin, resulting in the elongation of the mesocotyl and coleoptile of maize seedlings. A comprehensive evaluation analysis showed that the optimum concentration of 5-HT in relieving deep-seeding stress was 2.5 mg/L for both inbred lines, and 5-HT therefore could improve the seedling emergence rate and alleviate deep-seeding stress in maize seedlings. These findings could provide a novel strategy for improving maize deep-seeding tolerance, thus enhancing yield potential under drought and water stress. [ABSTRACT FROM AUTHOR]

Serotonin (5-HT), an indoleamine compound, has been known to mediate many physiological responses of plants under environmental stress. The deep-seeding (≥20 cm) of maize seeds is an important cultivation strategy to ensure seedling emergence and survival under drought stress. However, the role of 5-HT in maize deep-seeding tolerance remains unexplored. Understanding the mechanisms and evaluating the optimal concentration of 5-HT in alleviating deep-seeding stress could benefit maize production. In this study, two maize inbred lines were treated with or without 5-HT at both sowing depths of 20 cm and 3 cm, respectively. The effects of different concentrations of 5-HT on the growth phenotypes, physiological metabolism, and gene expression of two maize inbred lines were examined at the sowing depths of 20 cm and 3 cm. Compared to the normal seedling depth of 3 cm, the elongation of the mesocotyl (average elongation 3.70 cm) and coleoptile (average elongation 0.58 cm), secretion of indole-3-acetic acid (IAA; average increased 3.73 and 0.63 ng g−1 FW), and hydrogen peroxide (H2O2; average increased 1.95 and 0.63 μM g−1 FW) in the mesocotyl and coleoptile were increased under 20 cm stress, with a concomitant decrease in lignin synthesis (average decreased 0.48 and 0.53 A280 g−1). Under 20 cm deep-seeding stress, the addition of 5-HT activated the expression of multiple genes of IAA biosynthesis and signal transduction, including Zm00001d049601, Zm00001d039346, Zm00001d026530, and Zm00001d049659, and it also stimulated IAA production in both the mesocotyl and coleoptile of maize seedlings. On the contrary, 5-HT suppressed the expression of genes for lignin biosynthesis (Zm00001d016471, Zm00001d005998, Zm00001d032152, and Zm00001d053554) and retarded the accumulation of H2O2 and lignin, resulting in the elongation of the mesocotyl and coleoptile of maize seedlings. A comprehensive evaluation analysis showed that the optimum concentration of 5-HT in relieving deep-seeding stress was 2.5 mg/L for both inbred lines, and 5-HT therefore could improve the seedling emergence rate and alleviate deep-seeding stress in maize seedlings. These findings could provide a novel strategy for improving maize deep-seeding tolerance, thus enhancing yield potential under drought and water stress.

Summary: Shade affects all aspects of plant growth and development, including seed germination, hypocotyl elongation, petiole growth, leaf hyponasty, and flowering time. Here, we found that mutations in the key Arabidopsis karrikins signal perception‐associated KARRIKIN INSENSITIVE 2 (KAI2) gene, encoding an α/β‐fold hydrolase, and the MORE AXILLARY GROWTH 2 (MAX2) gene, encoding an F‐box protein, led to greater hypocotyl elongation under shade avoidance conditions.We further verified that these phenotypes were caused by perception of the endogenous KAI2‐ligands (KLs), and that this phenotype is independent of strigolactone biosynthetic or signaling pathways. Upon perception of a KL, it is probable that the target protein forms a complex with the KAI2/MAX2 proteins, which are degraded through the action of the 26S proteasome.We demonstrated that SUPPRESSOR OF MAX2‐1 (SMAX1) is the degradation target for the KAI2/MAX2 complex in the context of shade avoidance. KAI2 and MAX2 require SMAX1 to limit the hypocotyl growth associated with shade avoidance. Treatment with l‐kynurenine, an inhibitor of auxin accumulation, partially restored elongation of kai2 mutant hypocotyls under simulated shade. Furthermore, KAI2 is involved in regulating auxin accumulation and polar auxin transport, which may contribute to the hypocotyl shade response.In addition, SMAX1 gene overexpression promoted the hypocotyl shade response. RNA‐sequencing analysis revealed that SMAX1‐overexpression affected the expression of many auxin homeostasis genes, especially under simulated shade. Altogether, our data support the conclusion that KL signaling regulates shade avoidance by modulating auxin homeostasis in the hypocotyl. [ABSTRACT FROM AUTHOR]

After nitrogen treatments, plant leaves become narrower and thicker, and the chlorophyll content increases. However, the molecular mechanisms behind these regulations remain unknown. Here, we found that the changes in leaf width and thickness were largely compromised in the shade avoidance 3 (sav3) mutant. The SAV3 gene encodes an amino-transferase in the auxin biosynthesis pathway. Thus, the crosstalk between shade and nitrogen in Arabidopsis leaf development was investigated. Both hypocotyl elongation and leaf expansion promoted by the shade treatment were reduced by the high-N treatment; high-N-induced leaf narrowing and thickening were reduced by the shade treatment; and all of these developmental changes were largely compromised in the sav3 mutant. Shade treatment promoted SAV3 expression, while high-N treatment repressed SAV3 expression, which then increased or decreased auxin accumulation in cotyledons/leaves, respectively. SAV3 also regulates chlorophyll accumulation and nitrogen assimilation and thus may function as a master switch responsive to multiple environmental stimuli. [ABSTRACT FROM AUTHOR]

After nitrogen treatments, plant leaves become narrower and thicker, and the chlorophyll content increases. However, the molecular mechanisms behind these regulations remain unknown. Here, we found that the changes in leaf width and thickness were largely compromised in the shade avoidance 3 (sav3) mutant. The SAV3 gene encodes an amino-transferase in the auxin biosynthesis pathway. Thus, the crosstalk between shade and nitrogen in Arabidopsis leaf development was investigated. Both hypocotyl elongation and leaf expansion promoted by the shade treatment were reduced by the high-N treatment; high-N-induced leaf narrowing and thickening were reduced by the shade treatment; and all of these developmental changes were largely compromised in the sav3 mutant. Shade treatment promoted SAV3 expression, while high-N treatment repressed SAV3 expression, which then increased or decreased auxin accumulation in cotyledons/leaves, respectively. SAV3 also regulates chlorophyll accumulation and nitrogen assimilation and thus may function as a master switch responsive to multiple environmental stimuli.

Summary: The phytohormone auxin is essential for root development in plants. OsMADS25 is a homologue of the AGL17‐clade MADS‐box genes in rice. Despite recent progress, the molecular mechanisms underlying the regulation of root development by OsMADS25 are not well known. It is unclear whether OsMADS25 regulates root development via auxin signalling. In this study, we examined the role of OsMADS25 in root development and characterized the signalling pathway through which OsMADS25 regulates root system development in rice. OsMADS25 overexpression significantly increased, but RNAi gene silencing repressed primary root (PR) length and lateral root (LR) density. Moreover, OsMADS25 promoted LR development in response to NO3−. Further study showed that OsMADS25 increased auxin accumulation in the root system by enhancing auxin biosynthesis and transport, while also reducing auxin degradation, therefore stimulating root development. More importantly, OsMADS25 was found to regulate OsIAA14 expression directly by binding to the CArG‐box in the promoter region of OsIAA14, which encodes an Aux/indole acetic acid (IAA) transcriptional repressor of auxin signalling. Elevated auxin levels and decreased OsIAA14 expression might lead to reduced OsIAA14 protein accumulation, as a mechanism to regulate auxin signalling. Therefore, our findings reveal a molecular mechanism by which OsMADS25 modulates root system growth and development in rice, at least partilly, via Aux/IAA‐based auxin signalling. [ABSTRACT FROM AUTHOR]

Lanthanum (La) is one of rare earth elements that was used as a crop growth stimulants; however, high concentration of La markedly inhibited plant growth. Our previous study indicated that, although La induced the expression of auxin biosynthesis-related genes, it markedly repressed primary root (PR) elongation by reducing auxin accumulation in PR tips. In this study, we exhibited that La reduces the abundances of auxin carriers. Treatment with La markedly inhibited the auxins IAA-, 2,4-D-, and NAA-induced elevation of DR5:GUS activity in the roots, suggesting that La inhibited auxin transport through both the influx and efflux transporters. Supplementation with auxin transport inhibitor naphthylphthalamic acid in La-treated seedlings did not further reduce PR growth compared with that of the La treatment alone, further confirmed that auxin transport is involved in La-induced inhibition of PR growth. Analysis of the protein abundances using the transgenic AUX1-YFP and PIN1/2/4/7-GFP marker lines indicated that La treatment reduced the abundances of all these auxin carriers in the PR tips. La also increased the stabilization of Aux/IAA protein AXR3. Taken together, these results indicated that La treatment inhibits PIN-mediated auxin transport and subsequently impairs auxin distribution and PR growth via reducing auxin carrier abundances.

Mn toxicity inhibits both primary root (PR) growth and lateral root development. However, the mechanism underlying Mn-mediated root growth inhibition remains to be further elucidated. Here, we investigated the role of auxin in Mn-mediated inhibition of PR growth in Arabidopsis using physiological and genetic approaches. Mn toxicity inhibits PR elongation by reducing meristematic cell division potential. Mn toxicity also reduced auxin levels in root tips by reducing IAA biosynthesis and down-regulating the expression of auxin efflux carriers PIN4 and PIN7. Loss of function pin4 and pin7 mutants showed less inhibition of root growth than col-0 seedlings. These results indicated that this inhibitory effect of Mn toxicity on PR growth was mediated by affecting auxin biosynthesis and the expression of auxin efflux transporters PIN4 and PIN7. [ABSTRACT FROM AUTHOR]

In Arabidopsis thaliana in vitro culture, shoots were induced from the shoot apical meristem (SAM) of germinating seeds in the presence of 2,4-dichlorophenoxyacetic acid. Primary shoot primordia developed leaf-like structures, from which secondary shoot primordia were produced. Regenerated shoots were recovered when the material was transferred to a medium lacking auxin. Adventitious roots formed from a callusing basal region of the secondary shoots. The CUC1 transcription factor was expressed at the apex of the primary shoot primordium and at the boundary between the regenerated SAM and the developing leaf primordia. The DR5::GUS transgene was used to localize sites of maximum auxin occurrence. Auxin was firstly detected in the dividing cells beneath the SAM epidermis, which coincided with sites where primary shoot primordia were initiated. In the regenerated shoots, auxin response was not detected in the basal region of the stem, suggesting that the regenerating structures were shoots rather than somatic embryos. Direct shoot regeneration from the A. thaliana SAM requires a localized accumulation of auxin.

In Arabidopsis thaliana in vitro culture, shoots were induced from the shoot apical meristem (SAM) of germinating seeds in the presence of 2,4-dichlorophenoxyacetic acid. Primary shoot primordia developed leaf-like structures, from which secondary shoot primordia were produced. Regenerated shoots were recovered when the material was transferred to a medium lacking auxin. Adventitious roots formed from a callusing basal region of the secondary shoots. The CUC1 transcription factor was expressed at the apex of the primary shoot primordium and at the boundary between the regenerated SAM and the developing leaf primordia. The DR5::GUS transgene was used to localize sites of maximum auxin occurrence. Auxin was firstly detected in the dividing cells beneath the SAM epidermis, which coincided with sites where primary shoot primordia were initiated. In the regenerated shoots, auxin response was not detected in the basal region of the stem, suggesting that the regenerating structures were shoots rather than somatic embryos. Direct shoot regeneration from the A. thaliana SAM requires a localized accumulation of auxin. [ABSTRACT FROM AUTHOR]

The phytohormone ethylene plays important roles in regulating plant responses to phosphate (Pi) starvation. To date, however, no molecular components have been identified that interact with ethylene signalling in regulating such responses. In this work, an Arabidopsis mutant, hps4, was characterized that exhibits enhanced responses to Pi starvation, including increased inhibition of primary root growth, enhanced expression of Pi starvation-induced genes, and overproduction of root-associated acid phosphatases. Molecular cloning indicated that hps4 is a new allele of SABRE, which was previously identified as an important regulator of cell expansion in Arabidopsis. HPS4/SABRE antagonistically interacts with ethylene signalling to regulate plant responses to Pi starvation. Furthermore, it is shown that Pi-starved hps4 mutants accumulate more auxin in their root tips than the wild type, which may explain the increased inhibition of their primary root growth when grown under Pi deficiency. [ABSTRACT FROM AUTHOR]

Lanthanum (La) is one of rare earth elements that was used as a crop growth stimulants; however, high concentration of La markedly inhibited plant growth. Our previous study indicated that, although La induced the expression of auxin biosynthesis-related genes, it markedly repressed primary root (PR) elongation by reducing auxin accumulation in PR tips. In this study, we exhibited that La reduces the abundances of auxin carriers. Treatment with La markedly inhibited the auxins IAA-, 2,4-D-, and NAA-induced elevation of DR5:GUS activity in the roots, suggesting that La inhibited auxin transport through both the influx and efflux transporters. Supplementation with auxin transport inhibitor naphthylphthalamic acid in La-treated seedlings did not further reduce PR growth compared with that of the La treatment alone, further confirmed that auxin transport is involved in La-induced inhibition of PR growth. Analysis of the protein abundances using the transgenic AUX1-YFP and PIN1/2/4/7-GFP marker lines indicated that La treatment reduced the abundances of all these auxin carriers in the PR tips. La also increased the stabilization of Aux/IAA protein AXR3. Taken together, these results indicated that La treatment inhibits PIN-mediated auxin transport and subsequently impairs auxin distribution and PR growth via reducing auxin carrier abundances.

Mn toxicity inhibits both primary root (PR) growth and lateral root development. However, the mechanism underlying Mn-mediated root growth inhibition remains to be further elucidated. Here, we investigated the role of auxin in Mn-mediated inhibition of PR growth in Arabidopsis using physiological and genetic approaches. Mn toxicity inhibits PR elongation by reducing meristematic cell division potential. Mn toxicity also reduced auxin levels in root tips by reducing IAA biosynthesis and down-regulating the expression of auxin efflux carriers PIN4 and PIN7 . Loss of function pin4 and pin7 mutants showed less inhibition of root growth than col-0 seedlings. These results indicated that this inhibitory effect of Mn toxicity on PR growth was mediated by affecting auxin biosynthesis and the expression of auxin efflux transporters PIN4 and PIN7.