TGase-induced Cd tolerance by boosting polyamine, nitric oxide, cell wall composition and phytochelatin synthesis in tomato.

In highly intensive greenhouse vegetable production, soil acidification was caused by excessive fertilization, increasing cadmium (Cd) concentrations in the vegetables, which bears environmental hazards and is a negative influence on vegetables and humans. Transglutaminases (TGases), a central mediator for certain physiological effects of polyamines (PAs) in the plant kingdom, play important roles in plant development and stress response. Despite increased research on the crucial role of TGase in protecting against environmental stresses, relatively little is known about the mechanisms of Cd tolerance. In this study, we found, TGase activity and transcript level, which was upregulated by Cd, and TGase-induced Cd tolerance related to endogenous bound PAs increase and formation of nitric oxide (NO). Plant growth of tgase mutants was hypersensitive to Cd, chemical complementation by putrescine, sodium nitroprusside (SNP, nitric oxide donor) or gain of function TGase experiments restore Cd tolerance. α-diflouromethylornithine (DFMO, a selective ODC inhibitor) and 2-4-carboxyphenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO, NO scavenger), were respectively found declined drastically endogenous bound PA and NO content in TGase overexpression plants. Likewise, we reported that TGase interacted with polyamine uptake protein 3 (Put3), and the silencing of Put3 largely reduced TGase-induced Cd tolerance and bound PAs formation. This salvage strategy depends on TGase-regulated synthesis of bound PAs and NO that is able to positively increase the concentration of thiol and phytochelatins, elevate Cd in the cell wall, as well as induce the levels of expression Cd uptake and transport genes. Collectively, these findings indicate that TGase-mediated enhanced levels of bound PA and NO acts as a vital mechanism to protect the plant from Cd-caused toxicity.

Selenium Nanoparticles Mitigate Cadmium Stress in Tomato through Enhanced Accumulation and Transport of Sulfate/Selenite and Polyamines.

Accumulation of cadmium (Cd) ions in soil is an increasingly acute ecological problem in agriculture production. Selenium nanoparticles (SeNPs) can mediate Cd tolerance in plants; however, the underlying mechanisms remain unclear. Herein, we show that the foliar application of SeNPs improved the adaptive capacity of tomato plants to decrease Cd-induced damage. SeNPs induced more Cd in roots but not in shoots despite greater accumulation of selenium and sulfur in both tissues and high selenate influx. Additionally, SeNPs significantly increased thiol compounds, including glutathione, cysteine, and phytochelatins, contributing to enhanced Cd detoxification. Importantly, SeNPs induced the expression of sulfate transporters 1:3, S-adenosylmethionine 1 and polyamine transporter 3. Then, experiments with mutants of these genes showed that SeNP-reduced Cd stress largely relies on the levels and shoot-to-root transport of selenium/sulfur and polyamines. These findings highlight the potential of SeNPs to improve crop production and phytoremediation in heavy metal-contaminated soils.

MiR-33a plays an crucial role in the proliferation of bovine preadipocytes.

Preadipocyte proliferation is a critical and precisely orchestrated procedure in adipogenesis, which is highly regulated by microRNAs (miRNAs). A previous study identified that the expression of miR-33a is different in intramuscular fat (IMF) tissues from steers and bulls. In the present study, miR-33a was overexpressed in bovine preadipocytes, and a total of 781 differentialy expressed genes were found, including 348 upregulated and 433 downregulated genes. Gene Ontology and Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathway analyses of the differentially expressed genes enriched cell division and cell cycle respectively. MiR-33a overexpression decreased the rate of preadipocyte proliferation. Synchronously, the mRNA and protein expression levels of proliferation-related marker genes, including cyclin B1 (CCNB1) and proliferating cell nuclear antigen (PCNA), were decreased. In contrast, inhibiting miR-33a increased the rate of preadipocyte proliferation, and expression levels of CCNB1 and PCNA. Furthermore, based on luciferase reporter assays, miR-33a targeted directly cyclin-dependent kinase 6 (CDK6)-3'UTR and inhibited CDK6 protein expression. Interestingly, the silencing of CDK6 inhibited bovine preadipocyte proliferation and proliferation-related genes. Therefore, miR-33a inhibits the proliferation of bovine preadipocytes. CDK6 is the target gene of miR-33a and may be involved in the effects of miR-33a on bovine preadipocyte proliferation.