Abstract

BackgroundKiwifruit (Actinidia Lindl.) is considered an important fruit species worldwide. Due to its temperate origin, this species is highly vulnerable to freezing injury while under low-temperature stress. To obtain further knowledge of the mechanism underlying freezing tolerance, we carried out a hybrid transcriptome analysis of two A. arguta (Actinidi arguta) genotypes, KL and RB, whose freezing tolerance is high and low, respectively. Both genotypes were subjected to − 25 °C for 0 h, 1 h, and 4 h.ResultsSMRT (single-molecule real-time) RNA-seq data were assembled using the de novo method, producing 24,306 unigenes with an N50 value of 1834 bp. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis of DEGs showed that they were involved in the ‘starch and sucrose metabolism’, the ‘mitogen-activated protein kinase (MAPK) signaling pathway’, the ‘phosphatidylinositol signaling system’, the ‘inositol phosphate metabolism’, and the ‘plant hormone signal transduction’. In particular, for ‘starch and sucrose metabolism’, we identified 3 key genes involved in cellulose degradation, trehalose synthesis, and starch degradation processes. Moreover, the activities of beta-GC (beta-glucosidase), TPS (trehalose-6-phosphate synthase), and BAM (beta-amylase), encoded by the abovementioned 3 key genes, were enhanced by cold stress. Three transcription factors (TFs) belonging to the AP2/ERF, bHLH (basic helix-loop-helix), and MYB families were involved in the low-temperature response. Furthermore, weighted gene coexpression network analysis (WGCNA) indicated that beta-GC, TPS5, and BAM3.1 were the key genes involved in the cold response and were highly coexpressed together with the CBF3, MYC2, and MYB44 genes.ConclusionsCold stress led various changes in kiwifruit, the ‘phosphatidylinositol signaling system’, ‘inositol phosphate metabolism’, ‘MAPK signaling pathway’, ‘plant hormone signal transduction’, and ‘starch and sucrose metabolism’ processes were significantly affected by low temperature. Moreover, starch and sucrose metabolism may be the key pathway for tolerant kiwifruit to resist low temperature damages. These results increase our understanding of the complex mechanisms involved in the freezing tolerance of kiwifruit under cold stress and reveal a series of candidate genes for use in breeding new cultivars with enhanced freezing tolerance.

Highlights

  • Kiwifruit (Actinidia Lindl.) is considered an important fruit species worldwide

  • Cold stress led various changes in kiwifruit, the ‘phosphatidylinositol signaling system’, ‘inositol phosphate metabolism’, ‘mitogen-activated protein kinase (MAPK) signaling pathway’, ‘plant hormone signal transduction’, and ‘starch and sucrose metabolism’ processes were significantly affected by low temperature

  • Starch and sucrose metabolism may be the key pathway for tolerant kiwifruit to resist low temperature damages

Read more

Summary

Introduction

Kiwifruit (Actinidia Lindl.) is considered an important fruit species worldwide. Due to its temperate origin, this species is highly vulnerable to freezing injury while under low-temperature stress. Because plants are sessile organisms, low temperature can lead to decreased cell membrane fluidity and water potential and loss of protein function, resulting in enormous amounts of damage [3]. Throughout their long-term evolutionary development, plants have evolved a set of complex mechanisms to adapt to low temperatures [4]. SMRT long-read sequencing technology is currently becoming a popular method to obtain information on full-length (FL) mRNA molecules and has been extensively used for transcriptome profiling in various plant species [16,17,18,19]. The SMRT method cannot calculate the mapped number of reads to quantify the expression level of genes, but this problem can be solved with NGS (next-generation sequencing) technology [21]

Methods
Results
Discussion
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call