Background: As a cool-season grass species, tall fescue (Festuca arundinacea) is challenged by increasing temperatures. Heat acclimation or activation of leaf senescence, are two main strategies when tall fescue is exposed to heat stress (HS). However, lacking a genome sequence, the complexity of hexaploidy nature, and the short read of second-generation sequencing hinder a comprehensive understanding of the mechanism. This study aims to characterize the molecular mechanism of heat adaptation and heat-induced senescence at transcriptional and post-transcriptional levels. Results: Transcriptome of heat-treated (1 h and 72 h) and senescent leaves of tall fescue were generated by combining single-molecular real-time and Illumina sequencing. In total, 4076; 6917, and 11,918 differentially expressed genes (DEGs) were induced by short- and long-term heat stress (HS), and senescence, respectively. Venn and bioinformatics analyses of DEGs showed that short-term HS strongly activated heat shock proteins (Hsps) and heat shock factors (Hsfs), as well as specifically activated FK506-binding proteins (FKBPs), calcium signaling genes, glutathione S-transferase genes, photosynthesis-related genes, and phytohormone signaling genes. By contrast, long-term HS shared most of DEGs with senescence, including the up-regulated chlorophyll catabolic genes, phytohormone synthesis/degradation genes, stress-related genes, and NACs, and the down-regulated photosynthesis-related genes, FKBPs, and catalases. Subsequently, transient overexpression in tobacco showed that FaHsfA2a (up-regulated specifically by short-term HS) reduced cell membrane damages caused by HS, but FaNAC029 and FaNAM-B1 (up-regulated by long-term HS and senescence) increased the damages. Besides, alternative splicing was widely observed in HS and senescence responsive genes, including Hsps, Hsfs, and phytohormone signaling/synthesis genes. Conclusions: The short-term HS can stimulate gene responses and improve thermotolerance, but long-term HS is a damage and may accelerate leaf senescence. These results contribute to our understanding of the molecular mechanism underlying heat adaptation and heat-induced senescence.

Leaf senescence induced by prolonged light deficiency is inevitable whenever turfgrass is cultivated in forests, and this negatively influences the survival and aesthetic quality of the turfgrass. However, the mechanism underlying dark-induced senescence in turfgrass remained obscure. In this study, RNA sequencing was performed to analyze how genes were regulated in response to dark-induced leaf senescence in bermudagrass. A total of 159,207 unigenes were obtained with a mean length of 948 bp. The differential expression analysis showed that a total of 59,062 genes, including 52,382 up-regulated genes and 6680 down-regulated genes were found to be differentially expressed between control leaves and senescent leaves induced by darkness. Subsequent bioinformatics analysis showed that these differentially expressed genes (DEGs) were mainly related to plant hormone (ethylene, abscisic acid, jasmonic acid, auxin, cytokinin, gibberellin, and brassinosteroid) signal transduction, N-glycan biosynthesis, and protein processing in the endoplasmic reticulum. In addition, transcription factors, such as WRKY, NAC, HSF, and bHLH families were also responsive to dark-induced leaf senescence in bermudagrass. Finally, qRT-PCR analysis of six randomly selected DEGs validated the accuracy of sequencing results. Taken together, our results provide basic information of how genes respond to darkness, and contribute to the understanding of comprehensive mechanisms of dark-induced leaf senescence in turfgrass.

Temperature sensitivity and tolerance play a key role in plant survival and production. Perennial ryegrass (Lolium perenne L.), widely cultivated in cool‐season for forage supply and turfgrass, is extremely susceptible to high temperatures, therefore serving as an excellent grass for dissecting the genomic and genetic basis of high‐temperature adaptation. In this study, expression analysis revealed that LpHsfA2, an important gene associated with high‐temperature tolerance in perennial ryegrass, is rapidly and substantially induced under heat stress. Additionally, heat‐tolerant varieties consistently display elevated expression levels of LpHsfA2 compared with heat‐sensitive ones. Comparative haplotype analysis of the LpHsfA2 promoter indicated an uneven distribution of two haplotypes (HsfA2^Hap1 and HsfA2^Hap2) across varieties with differing heat tolerance. Specifically, the HsfA2^Hap1 allele is predominantly present in heat‐tolerant varieties, while the HsfA2^Hap2 allele exhibits the opposite pattern. Overexpression of LpHsfA2 confers enhanced thermotolerance, whereas silencing of LpHsfA2 compromises heat tolerance. Furthermore, LpHsfA2 orchestrates its protective effects by directly binding to the promoters of LpHSP18.2 and LpAPX1 to activate their expression, preventing the non‐specific misfolding of intracellular protein and the accumulation of reactive oxygen species in cells. Additionally, LpHsfA4 and LpHsfA5 were shown to engage directly with the promoter of LpHsfA2, upregulating its expression as well as the expression of LpHSP18.2 and LpAPX1, thus contributing to enhanced heat tolerance. Markedly, LpHsfA2 possesses autoregulatory ability by directly binding to its own promoter to modulate the self‐transcription. Based on these findings, we propose a model for modulating the thermotolerance of perennial ryegrass by precisely regulating the expression of LpHsfA2. Collectively, these findings provide a scientific basis for the development of thermotolerant perennial ryegrass cultivars.