The rapid development of omics sequencing technology has facilitated the identification of thousands of long non-coding (lnc)RNAs in plant species, but the role of lncRNAs in plant-pathogen interactions remains largely unexplored. We used comparative transcriptome analysis of Phytophthora infestans-resistant and -susceptible tomatoes to identify differentially expressed genes (DEGs) and lncRNAs (DELs), and examine lncRNA-mRNA networks. A total of 1037 DEGs and 688 DELs were identified between P. infestans-resistant and -susceptible tomatoes. The co-localization networks, including 128 DEGs and 127 DELs, were performed. We found that lncRNA16397 acted as an antisense transcript of SlGRX22 to regulate its expression, and also induced SlGRX21 expression when lncRNA16397 was overexpressed. In addition, disease symptoms and reactive oxygen species (ROS) accumulation in tomatoes overexpressing lncRNA16397 and SpGRX were fewer and lower than those in wild-type after P. infestans infection. This result suggests that tomato lncRNA16397 induces SlGRX expression to reduce ROS accumulation and alleviate cell membrane injury, resulting in enhanced resistance to P. infestans. Our results provide insight into lncRNAs involved in the response of tomato to P. infestans infection, demonstrate that the lncRNA16397-GRXs network is an important component of the P. infestans network in tomato, and provide candidates for breeding to enhance biotic stress-resistance in tomato.

Our previous studies indicated that tomato miR482b could negatively regulate the resistance of tomato to Phytophthora infestans and the expression of miR482b was decreased after inoculation with P. infestans. However, the mechanism by which the accumulation of miR482b is suppressed remains unclear. In this study, we wrote a program to identify 89 long noncoding RNA (lncRNA)-originated endogenous target mimics (eTMs) for 46 miRNAs from our RNA-Seq data. Three tomato lncRNAs, lncRNA23468, lncRNA01308 and lncRNA13262, contained conserved eTM sites for miR482b. When lncRNA23468 was overexpressed in tomato, miR482b expression was significantly decreased, and the expression of the target genes, NBS-LRRs, was significantly increased, resulting in enhanced resistance to P. infestans. Silencing lncRNA23468 in tomato led to the increased accumulation of miR482b and decreased accumulation of NBS-LRRs, as well as reduced resistance to P. infestans. In addition, the accumulation of both miR482b and NBS-LRRs was not significantly changed in tomato plants that overexpressed lncRNA23468 with a mutated eTM site. Based on the VIGS system, a target gene of miR482b, Solyc02g036270.2, was silenced. The disease symptoms of the VIGS-Solyc02g036270.2 tomato plants were in accordance with those of tomato plants in which lncRNA23468 was silenced after inoculation with P. infestans. More severe disease symptoms were found in the modified plants than in the control plants. Our results demonstrate that lncRNAs functioning as eTMs may modulate the effects of miRNAs in tomato and provide insight into how the lncRNA23468-miR482b-NBS-LRR module regulates tomato resistance to P. infestans.

Approximately 50% of patients with primary colorectal carcinoma develop liver metastases. Understanding the genetic differences between primary colon cancer and their metastases to the liver is essential for devising a better therapeutic approach for this disease. We performed whole exome sequencing and copy number analysis for 15 triplets, each comprising normal colorectal tissue, primary colorectal carcinoma, and its synchronous matched liver metastasis. We analyzed the similarities and differences between primary colorectal carcinoma and matched liver metastases in regards to somatic mutations and somatic copy number alterationss. The genomic profiling demonstrated mutations in APC(73%), KRAS (33%), ARID1A and PIK3CA (6.7%) genes between primary colorectal and metastatic liver tumors. TP53 mutation was observed in 47% of the primary samples and 67% in liver metastatic samples. The grouped pairs, in hierarchical clustering showed similar somatic copy number alteration patterns, in contrast to the ungrouped pairs. Many mutations (including those of known key cancer driver genes) were shared in the grouped pairs. The ungrouped pairs exhibited distinct mutation patterns with no shared mutations in key driver genes. Four ungrouped liver metastasis samples had mutations in DNA mismatch repair genes along with hypermutations and a substantial number of copy number alterations. Our results suggest that about half of the metastatic colorectal carcinoma had the same clonal origin with their primary colorectal carcinomas, whereas remaining cases were genetically distinct from their primary carcinomas. These findings underscore the need to evaluate metastatic lesions separately for optimized therapy, rather than to extrapolate from primary tumor data.