BackgroundBamboo occupies an important phylogenetic node in the grass family with remarkable sizes, woodiness and a striking life history. However, limited genetic research has focused on bamboo partially because of the lack of genomic resources. The advent of high-throughput sequencing technologies enables generation of genomic resources in a short time and at a minimal cost, and therefore provides a turning point for bamboo research. In the present study, we performed de novo transcriptome sequencing for the first time to produce a comprehensive dataset for the Ma bamboo (Dendrocalamus latiflorus Munro).ResultsThe Ma bamboo transcriptome was sequenced using the Illumina paired-end sequencing technology. We produced 15,138,726 reads and assembled them into 103,354 scaffolds. A total of 68,229 unigenes were identified, among which 46,087 were annotated in the NCBI non-redundant protein database and 28,165 were annotated in the Swiss-Prot database. Of these annotated unigenes, 11,921 and 10,147 unigenes were assigned to gene ontology categories and clusters of orthologous groups, respectively. We could map 45,649 unigenes onto 292 pathways using the Kyoto Encyclopedia of Genes and Genomes Pathway database. The annotated unigenes were compared against Moso bamboo, rice and millet. Unigenes that did not match any of those three sequence datasets are considered to be Ma bamboo unique. We predicted 105 unigenes encoding eight key enzymes involved in lignin biosynthesis. In addition, 621 simple sequence repeats (SSRs) were detected.ConclusionOur data provide the most comprehensive transcriptomic resource currently available for D. latiflorus Munro. Candidate genes potentially involved in growth and development were identified, and those predicted to be unique to Ma bamboo are expected to give a better insight on Ma bamboo gene diversity. Numerous SSRs characterized contributed to marker development. These data constitute a new valuable resource for genomic studies on D. latiflorus Munro and, more generally, bamboo.

SummaryThe hyperaccumulating ecotype of Sedum alfredii Hance is a cadmium (Cd)/zinc/lead co‐hyperaccumulating species of Crassulaceae. It is a promising phytoremediation candidate accumulating substantial heavy metal ions without obvious signs of poisoning. However, few studies have focused on the regulatory roles of miRNAs and their targets in the hyperaccumulating ecotype of S. alfredii. Here, we combined analyses of the transcriptomics, sRNAs and the degradome to generate a comprehensive resource focused on identifying key regulatory miRNA‐target circuits under Cd stress. A total of 87 721 unigenes and 356 miRNAs were identified by deep sequencing, and 79 miRNAs were differentially expressed under Cd stress. Furthermore, 754 target genes of 194 miRNAs were validated by degradome sequencing. A gene ontology (GO) enrichment analysis of differential miRNA targets revealed that auxin, redox‐related secondary metabolism and metal transport pathways responded to Cd stress. An integrated analysis uncovered 39 pairs of miRNA targets that displayed negatively correlated expression profiles. Ten miRNA‐target pairs also exhibited negative correlations according to a real‐time quantitative PCR analysis. Moreover, a coexpression regulatory network was constructed based on profiles of differentially expressed genes. Two hub genes, ARF4 (auxin response factor 4) and AAP3 (amino acid permease 3), which might play central roles in the regulation of Cd‐responsive genes, were uncovered. These results suggest that comprehensive analyses of the transcriptomics, sRNAs and the degradome provided a useful platform for investigating Cd hyperaccumulation in S. alfredii, and may provide new insights into the genetic engineering of phytoremediation.

Cardiorenal syndrome type 4 (CRS4) is a common complication of chronic kidney disease (CKD), but the pathogenic mechanisms remain elusive. Here we report that morphological and functional changes in myocardial mitochondria are observed in CKD mice, especially decreases in oxidative phosphorylation and fatty acid metabolism. High phosphate (HP), a hallmark of CKD, contributes to myocardial energy metabolism dysfunction by downregulating peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC1α). Furthermore, the transcriptional factor interferon regulatory factor 1 (IRF1) is revealed as the key molecule upregulated by HP through histone H3K9 acetylation, and responsible for the HP-mediated transcriptional inhibition of PGC1α by directly binding to its promoter region. Conversely, restoration of PGC1α expression or genetic knockdown of IRF1 significantly attenuates HP-induced alterations in vitro and in vivo. These findings demonstrate that IRF1-PGC1α axis-mediated myocardial energy metabolism remodeling plays a crucial role in the pathogenesis of CRS4.