An Overview of Plant Response to Salt Stress: About hormone signaling pathway

Soil salinity is a major abiotic stress that limits plant growth and productivity. High concentrations of sodium chloride can cause osmotic and ionic effects. This stress minimises a plant’s ability to uptake water and minerals, and increases Na+ accumulation in the cytosol, thereby disturbing metabolic processes. Prolonged plant exposure to salt stress can lead to oxidative stress and increased production of reactive oxygen species (ROS). Higher plants developed some strategies to cope with salt stress. Among these, mechanisms involving nitric oxide (NO) and polyamines (PAs) are particularly important. NO is a key signalling molecule that mediates a variety of physiological functions and defence responses against abiotic stresses in plants. Under salinity conditions, NO donors increase growth parameters, reduce Na+ toxicity, maintain ionic homeostasis, stimulate osmolyte accumulation and prevent damages caused by ROS. NO enhances salt tolerance of plants via post-translational protein modifications through S-nitrosylation of thiol groups, nitration of tyrosine residues and modulation of multiple gene expression. Several reviews have reported on the role of polyamines in modulating salt stress plant response and the capacity to enhance PA synthesis upon salt stress exposure, and it is known that NO and PAs interact under salinity. In this review, we focus on the role of NO in plant response to salt stress, paying particular attention to the interaction between NO and PAs.

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TaSnRK2.9, a Sucrose Non-fermenting 1-Related Protein Kinase Gene, Positively Regulates Plant Response to Drought and Salt Stress in Transgenic Tobacco

Frontiers in Plant Science ◽

10.3389/fpls.2018.02003 ◽

2019 ◽

Vol 9 ◽

Cited By ~ 7

Author(s):

Jialu Feng ◽

Lianzhe Wang ◽

Yanan Wu ◽

Qingchen Luo ◽

Yang Zhang ◽

...

Keyword(s):

Salt Stress ◽

Protein Kinase ◽

Transgenic Tobacco ◽

Plant Response ◽

Related Protein ◽

Kinase Gene ◽

Drought And Salt Stress ◽

Protein Kinase Gene

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MiR-2 family regulates insect metamorphosis by controlling the juvenile hormone signaling pathway

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1418522112 ◽

2015 ◽

Vol 112 (12) ◽

pp. 3740-3745 ◽

Cited By ~ 53

Author(s):

Jesus Lozano ◽

Raúl Montañez ◽

Xavier Belles

Keyword(s):

Transcription Factor ◽

Juvenile Hormone ◽

Binding Site ◽

Signaling Pathway ◽

Blattella Germanica ◽

Mrna Levels ◽

Hormone Signaling ◽

Nymphal Instar ◽

Insect Metamorphosis ◽

Krüppel Homolog 1

In 2009 we reported that depletion of Dicer-1, the enzyme that catalyzes the final step of miRNA biosynthesis, prevents metamorphosis inBlattella germanica. However, the precise regulatory roles of miRNAs in the process have remained elusive. In the present work, we have observed that Dicer-1 depletion results in an increase of mRNA levels of Krüppel homolog 1 (Kr-h1), a juvenile hormone-dependent transcription factor that represses metamorphosis, and that depletion of Kr-h1 expression in Dicer-1 knockdown individuals rescues metamorphosis. We have also found that the 3′UTR of Kr-h1 mRNA contains a functional binding site for miR-2 family miRNAs (for miR-2, miR-13a, and miR-13b). These data suggest that metamorphosis impairment caused by Dicer-1 and miRNA depletion is due to a deregulation of Kr-h1 expression and that this deregulation is derived from a deficiency of miR-2 miRNAs. We corroborated this by treating the last nymphal instar ofB. germanicawith an miR-2 inhibitor, which impaired metamorphosis, and by treating Dicer-1-depleted individuals with an miR-2 mimic to allow nymphal-to-adult metamorphosis to proceed. Taken together, the data indicate that miR-2 miRNAs scavenge Kr-h1 transcripts when the transition from nymph to adult should be taking place, thus crucially contributing to the correct culmination of metamorphosis.

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