Thomas Blein

As sessile organisms, plants are continuously exposed to heterogeneous and changing environments and constantly need to adapt their growth strategies. They have evolved complex mechanisms to recognize various stress factors, activate appropriate signaling pathways, and respond accordingly by reprogramming the expression of multiple genes at the transcriptional, post-transcriptional, and even epigenome levels to tolerate stressful conditions such as drought, high temperature, nutrient deficiency, and pathogenic interactions. Apart from protein-coding genes, long non-coding RNAs (lncRNAs) have emerged as key players in plant adaptation to environmental stresses. They are transcripts larger than 200 nucleotides without protein-coding potential. Still, they appear to regulate a wide range of processes, including epigenetic modifications and chromatin reorganization, as well as transcriptional and post-transcriptional modulation of gene expression, allowing plant adaptation to various environmental stresses. LncRNAs can positively or negatively modulate stress responses, affecting processes such as hormone signaling, temperature tolerance, and nutrient deficiency adaptation. Moreover, they also seem to play a role in stress memory, wherein prior exposure to mild stress enhances plant ability to adapt to subsequent stressful conditions. In this review, we summarize the contribution of lncRNAs in plant adaptation to biotic and abiotic stresses, as well as stress memory. The complex evolutionary conservation of lncRNAs is also discussed and provides insights into future research directions in this field.

Besides regulating splicing, the conserved spliceosome component SmD1 (Small nuclear ribonucleoprotein D1)b promotes posttranscriptional silencing of sense transgenes (S-PTGS [post-transcriptional genesilencing]). Here, we show that the conserved spliceosome component PRP39 (Pre-mRNA-processing factor 39)a also plays a role in S-PTGS in Arabidopsis thaliana. However, PRP39a and SmD1b actions appear distinct in both splicing and S-PTGS. Indeed, RNAseq-based analysis of expression level and alternative splicing in prp39a and smd1b mutants identified different sets of deregulated transcripts and noncoding RNAs. Moreover, double mutant analyses involving prp39a or smd1b and RNA quality control (RQC) mutants revealed distinct genetic interactions for SmD1b and PRP39a with nuclear RQC machineries, suggesting nonredundant roles in the RQC/PTGS interplay. Supporting this hypothesis, a prp39a smd1b double mutant exhibited enhanced suppression of S-PTGS compared to the single mutants. Because the prp39a and smd1b mutants (i) showed no major changes in the expression of PTGS or RQC components or in small RNA production and (ii) do not alter PTGS triggered by inverted-repeat transgenes directly producing dsRNA (IR-PTGS), PRP39a, and SmD1b appear to synergistically promote a step specific to S-PTGS. We propose that, independently from their specific roles in splicing, PRP39a and SmD1b limit 3′-to-5′ and/or 5′-to-3′ degradation of transgene-derived aberrant RNAs in the nucleus, thus favoring the export of aberrant RNAs to the cytoplasm where their conversion into double-stranded RNA (dsRNA) initiates S-PTGS.