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ABSTRACT: Soil microorganisms in saline-alkali degraded grassland.

PROVIDER: PRJNA907217 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22477854_1.fastq.gz	Fastqsanger.gz
	SRR22477854_2.fastq.gz	Fastqsanger.gz
	SRR22477855_1.fastq.gz	Fastqsanger.gz
	SRR22477855_2.fastq.gz	Fastqsanger.gz
	SRR22477856_1.fastq.gz	Fastqsanger.gz

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Melatonin confers saline-alkali tolerance by relieving nitrosative damage and S-nitrosylation of plasma membrane H+-ATPase 2 in tomato

Project description:Soil salination and alkalization are global problems impairing plant survival by disrupting REDOX homeostasis. Whether melatonin regulates REDOX homeostasis at nitrosative level, and thus affects plant saline-alkali tolerance remains unknown. In saline-alkali stress, excess nitric oxide (NO) causes nitrosative damage in tomato roots. This NO can be degraded by S-nitrosoglutathione reductase (GSNOR), or stimulates caffeic acid O-methyltransferase (COMT) transcript for melatonin synthesis. Melatonin further feedback scavenges excess NO to alleviate nitrosative damage at the whole protein level, indicating by proteome S-nitrosylation. We target plasma membrane H+-ATPase 2 (HA2) and highlight that HA2 is S-nitrosylated at Cys206 in saline-alkali stress, reducing HA activity, H+ efflux, and tolerance by impairing its interaction with 14-3-3 protein 1 (TFT1). In agreement with these observations, COMT-mediated melatonin relieves the HA2 S-nitrosylation to recover its function and saline-alkali tolerance. Therefore, we propose NO and melatonin as a pair of REDOX switches to control HA2 S-nitrosylation and saline-alkali tolerance. Under natural saline-alkali conditions, tomato productivity can be improved by grafting with COMT-, GSNOR-, HA2-overexpression rootstocks or by genetic engineering non-nitrosylated HA2C206S mutants. Using melatonin-NO-HA2 module as a case, this study illuminates a novel molecular function of melatonin and relevant genetic engineering strategies in future agriculture.

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Project description:Salt stress, especially saline-alkali stress, has seriously negative effect on citrus production. Ziyang xiangcheng (Citrus junos Sieb.) (Cj) has been reported as a saline-alkali stress and iron deficiency tolerant citrus rootstock. However, the molecular mechanism of its saline-alkali stress tolerance is still not clear. Two citrus rootstocks and one navel orange scion, Cj, Poncirus trifoliate (Poncirus trifoliata (L.) Raf.) (Pt) and ‘Lane Late’ navel orange (Citrus sinensis (L.) Osb.) (LL), were used in this study. The grafted materials Cj+LL and Pt+LL grown in calcareous soil were used to identify genes and pathways responsive to saline-alkali stress using RNA-seq. The seedlings of Cj and Pt grown in the solutions with different gradient pH value were used to perform a supplement experiment. Comprehensively analyzing the data of RNA-seq, physiology and biochemistry, agronomic traits and mineral elements of Cj+LL, Pt+LL, Cj and Pt, several candidate pathways and genes were identified to be highly regulated under saline-alkali stress. Here, we propose citrate is important for the tolerance to iron deficiency and the jasmonate (JA) biosynthesis and signal transduction pathway may play a crucial role in tolerance to saline-alkali stress in citrus by interacting with other plant hormones, calcium signaling, ROS scavenging system and lignin biosynthesis.

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