Efficient assembly of nanopore reads via highly accurate and intact error correction.

Long nanopore reads are advantageous in de novo genome assembly. However, nanopore reads usually have broad error distribution and high-error-rate subsequences. Existing error correction tools cannot correct nanopore reads efficiently and effectively. Most methods trim high-error-rate subsequences during error correction, which reduces both the length of the reads and contiguity of the final assembly. Here, we develop an error correction, and de novo assembly tool designed to overcome complex errors in nanopore reads. We propose an adaptive read selection and two-step progressive method to quickly correct nanopore reads to high accuracy. We introduce a two-stage assembler to utilize the full length of nanopore reads. Our tool achieves superior performance in both error correction and de novo assembling nanopore reads. It requires only 8122 hours to assemble a 35X coverage human genome and achieves a 2.47-fold improvement in NG50. Furthermore, our assembly of the human WERI cell line shows an NG50 of 22 Mbp. The high-quality assembly of nanopore reads can significantly reduce false positives in structure variation detection.

MicroRNA-497 promotes proliferation and inhibits apoptosis of cardiomyocytes through the downregulation of Mfn2 in a mouse model of myocardial ischemia-reperfusion injury.

INTRODUCTION: Myocardial ischemia-reperfusion (I/R) injury affects millions of people worldwide and has a very high mortality rate. Since microRNA-497 (miR-497) has been found to be related with cardiomyocyte apoptosis, this study aimed to explore the effect of miR-497 by targeting Mfn2 in a mouse model of myocardial ischemia-reperfusion (I/R) injury. MATERIALS: BALB/c mice were modeled with I/R and some were injected with miR-497 agomir before I/R to observe whether miR-497 alleviates the injury that occurs as a result of I/R. Bioinformatics website and dual-luciferase reporter gene assay were employed in order to detect the relations between miR-497 and Mfn2 gene. Next, cells were extracted to be transfected with different mimic, inhibitor and siRNAs to further explore how miR-497 acts to I/R. Western blot analysis and reverse transcription quantitative polymerase chain reaction (RT-qPCR) were conducted to measure expressions of miR-497, Mfn2, Fas, Bcl-2, Bax and Caspase-3 in myocardial tissues and cardiomyocytes after transfection. CCK-8 assay and flow cytometry were used to determine proliferation, cell cycle distribution and apoptosis of cardiomyocytes in each group after transfection. RESULTS: Mice with I/R had myocardial dysfunction but before the injection with miR-497 agomir, the impairment was alleviated. Mfn2 was verified as the target gene of miR-497. The inhibition of miR-497 in turn inhibits Mfn2 expressione and cardiomyocyte apoptosis. The overexpression of miR-497 and Mfn2 gene silencing can lead to the promotion of proliferation capability of mice cardiomyocytes in vitro. Overexpressed miR-497 and Mfn2 gene silencing can also facilitate cell cycle entry and inhibit the apoptosis cardiomyocytes of mice in vitro. CONCLUSION: The present study provided strong evidence that miR-497 promotes proliferation and inhibits apoptosis of cardiomyocytes by downregulating the expression of Mfn2 in a mouse model of myocardial I/R injury.