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Background Polyamine and ethylene biosynthesis pathway genes are widely involved in the regulation of plant abiotic stresses. For their biosynthesis, both pathways require the same precursor, Synthase Adenosyl Methionine (SAM) enzyme. Whether they function as competitors or collaborators to regulate plant abiotic stress tolerance is still an elusive topic. Genome wide analysis of Cleistogenes songorica polyamine and ethylene pathway gene families was conducted to study their evolutionary relationship. And, using Arabidopsis plants transformed with a polyamine gene SAMDC2 from C. songorica, the expression of key genes from both pathways, and other previously well-studied stress responsive genes was investigated under salt or drought stress. Further, the ABA’s role on this interaction salt stress was also studied. Results 17 polyamine, 12 ethylene and 6 SAM biosynthesis related genes were identified at genome wide level in C. songorica. Phylogenetic analysis revealed close evolutionary similarities between gene families from both pathways. Also, analysis of cis regulatory elements indicated that SAM family genes promoters were rich into both ABA and ethylene related cis regulatory elements. Transcriptomic analysis, qRT-PCR validation, and confirmation using transgenic Arabidopsis showed that polyamine and ethylene key pathway genes can be concurrently expressed during abiotic stresses. Arabidopsis plants expressing a polyamine gene CsSAMDC2 driven by RD29A showed an improved drought and salt stress tolerance, and an increased expression of key polyamine and ethylene pathway genes. These plants maintained higher chlorophyll content and photosynthetic capacity. Morphological analysis of transgenic seedlings showed that leaves of these lines exhibited a more compact architecture following salt stress exposure. Application of ABA on transgenic lines under salt stress further improved the expression of polyamine and ethylene pathway genes. Further, lateral and primary root development were found improved during salt stress and ABA treatments. Interestingly, the expression of ethylene pathway genes was not reversed by exogenous ABA during salt stress treatment. Conclusion In silico and gene functional analysis assays revealed potential evolutionary and functional similarities between polyamine and ethylene pathway gene families. Such findings imply a synergetic interaction between polyamine and ethylene pathways, and the significant role of ABA on this crosstalk.

Genome-wide association studies (GWAS) have identified and reproduced thousands of diseases associated loci but many of them are not directly interpretable due to the strong linkage disequilibrium among variants. Transcriptome-wide association studies (TWAS) incorporated expression quantitative trait loci (eQTL) cohorts as reference panel to detect associations with the phenotype at the gene level and were gaining popularity in recent years. For nicotine addiction, several important susceptible genetic variants were identified by GWAS, but TWAS that detected genes associated with nicotine addiction and unveiled the underlying molecular mechanism were still lacking. In this study, we used eQTL data from the Genotype-Tissue Expression (GTEx) consortium as reference panel to conduct tissue specific TWAS on cigarettes per day (CPD) over 13 brain tissues in two large cohorts: UK Biobank (UKBB; N=142,202) and the GWAS & Sequencing Consortium of Alcohol and Nicotine use (GSCAN; N=143,210), and then meta-analyzed the results across tissues while considering the heterogeneity across tissues. We identified three major clusters of genes with different meta-patterns across tissues consistent in both cohorts, including homogenous genes associated with CPD in all brain tissues, partially homogeneous genes associated with CPD in cortex, cerebellum and hippocampus tissues, and lastly the tissue-specific genes associated with CPD in only few specific brain tissues. Downstream enrichment analyses on each gene cluster identified unique biological pathways associated with CPD and provided important biological insights into the regulatory mechanism of nicotine dependence in the brain.