In plants, salicylic acid (SA) is a signaling molecule that regulates disease resistance responses, such as systemic acquired resistance (SAR) and hypertensive response (HR). SA has been implicated as participating in various biotic and abiotic stresses. This study was conducted to investigate the role of SA in adventitious root formation (ARF) in mung bean (Phaseolus radiatus L) hypocotyl cuttings. We observed that hypocotyl treatment with SA could significantly promote the adventitious root formation, and its effects were dose and time dependent. Explants treated with SA displayed a 130% increase in adventitious root number compared with control seedlings. The role of SA in mung bean hypocotyl ARF as well as its interaction with hydrogen peroxide (H2O2) were also elucidated. Pretreatment of mung bean explants with N, N’-dimethylthiourea (DMTU), a scavenger for H2O2, resulted in a significant reduction of SA-induced ARF. Diphenyleneiodonium (DPI), a specific inhibitor of membrane-linked NADPH oxidase, also inhibited the effect of adventitious rooting triggered by SA treatment. The determination of the endogenous H2O2 level indicated that the seedlings treated with SA could induce H2O2 accumulation compared with the control treatment. Our results revealed a distinctive role of SA in the promotion of adventitious rooting via the process of H2O2 accumulation. This conclusion was further supported by antioxidant enzyme activity assays. Based on these results, we conclude that the accumulation of free H2O2 might be a downstream event in response to SA-triggered adventitious root formation in mung bean seedlings.
Cytoplasmic male sterile (CMS) rice Zhenshan 97A (ZS97A) has been widely used in hybrid rice production in China. However, ZS97A suffers from serious panicle enclosure, which blocks normal pollination and greatly reduces seed production of hybrid rice. Little is known about the cause of panicle closure in ZS97A. In this study, it was found that the occurrence of cytoplasmic male sterility caused a deficiency of indole-3-acetic acid (IAA) in ZS97A panicles, and less IAA was provided to the uppermost internode (UI). Further, it was found that the decreased panicle-derived IAA caused a gibberellin A(1) (GA(1)) deficiency in the UI by the down-regulation of OsGA3ox2 transcript level. Reduced GA(1) level in the UI led to decreases of both cell number and cell elongation, resulting in a shortened UI. The shortened UI was unable to push the panicle out of the flag leaf sheath that remained normal, which resulted in panicle enclosure in ZS97A. These findings suggest that decreased panicle-derived IAA reduces the GA(1) level in the UI, causing panicle enclosure in CMS rice ZS97A.
We used auxin-signalling mutants, auxin transport mutants, and auxin-related marker lines to show that exogenously applied GA enhances auxin-induced root inhibition by affecting auxin signalling and transport. Variation in root elongation is valuable when studying the interactions of phytohormones. Auxins influence the biosynthesis and signalling of gibberellins (GAs), but the influence of GAs on auxins in root elongation is poorly understood. This study was conducted to investigate the effect of GA3 on Arabidopsis root elongation in the presence of auxin. Root elongation was inhibited in roots treated with both IAA and GA3, compared to IAA alone, and the effect was dose dependent. Further experiments showed that GA3 could modulate auxin signalling based on root elongation in auxin-signalling mutants and the expression of auxin-responsive reporters. The GA3-enhanced inhibition of root elongation observed in the wild type was not found in the auxin-signalling mutants tir1-1 and axr1-3. GA3 increased DR5::GUS expression in the root meristem and elongation zones, and IAA2::GUS in the columella. The DR5rev::GFP signal was enhanced in columella cells of the root caps and in the elongation zone in GA3-treated seedling roots. A reduction was observed in the stele of PAC-treated roots. We also examined the effect of GA3 on auxin transport. The enhanced responsiveness caused by GA3 was not observed in the auxin influx mutant aux1-7 or the efflux mutant eir1-1. Additional molecular data demonstrated that GA3 could promote auxin transport via AUX1 and PIN proteins. However, GA3-induced PIN gene expression did not fully explain GA-enhanced PIN protein accumulation. These results suggest that GA3 is involved in auxin-mediated primary root elongation by modulating auxin signalling and transport, and thus enhances root responsiveness to exogenous IAA.
Root hair development is orchestrated by nutritional factors and plant hormones. We investigated the action of ammonium (NH 4 + ) and its interactions with methyl jasmonate (MeJA) and ethylene in Arabidopsis root hair growth. The formation of root hair branches was dramatically stimulated in media containing 1.25 to 20 mM NH 4 + at pH values of 4.0 to 6.5. The NH 4 + -treated root hairs showed a very short tip growth stage and swells on the sides that indicated the emergence of branches. MeJA (0.08 to 10 μM) worked in synergism with NH 4 + to enhance hair branching. In contrast, ethylene had an antagonistic effect; the stimulation of hair branching by NH 4 + was suppressed by the ethylene precursor 1-aminocyclopropane-1-carboxylic acid (ACC) and was diminished in ethylene-overproducing mutant eto1-1 seedlings. Moreover, the application of Ag + , an ethylene inhibitor, reduced the ACC-induced inhibition of NH 4 + -stimulated hair branching and restored NH 4 + -stimulated hair branching in eto1-1 seedlings. Thus, the actions of jasmonate and ethylene appear to be dependent on nutritional conditions such as available nitrogen.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.