scholarly journals MicroRNA319-mediated gene regulatory network impacts leaf development and morphogenesis in poplar

2021 ◽  
Vol 1 (1) ◽  
pp. 1-10
Author(s):  
Yanxia Cheng ◽  
◽  
Lihu Wang ◽  
Manzar Abbas ◽  
Xiong Huang ◽  
...  
2020 ◽  
Author(s):  
Xizhi Li ◽  
Min Li ◽  
Beibei Zhou ◽  
Jinlin Bao ◽  
Liang Zhu ◽  
...  

Abstract Background SRL1 (SEMI-ROLLED LEAF 1) also named as CLD1 (CURLED LEAF AND DWARF 1), encoding a putative glyphopholipidininol-anchored membrane protein, has been characterized as a gene involved in the regulation of leaf morphology in rice. Mutants of srl1-1 (point mutation) and srl1-2 (transferred DNA insertion) exhibit defects in leaf development resulting in a phenotype with adaxially rolled leaves. Results To explore the gene regulatory network of leaf development that controlled by SRL1 in rice, we created a homozygous SRL1 knock out (KO) line by CRISPR/Cas9, which showed defects in leaf development with adaxially rolling. By comparing the leaf transcriptome of a homozygous SRL1 KO line (srl1-KO) with the control, a total number of 3,178 genes were identified as differentially expressed genes, of which 1,216 genes were significantly up regulated, while 1,962 genes were down regulated. Further analyses indicated that, a group of known leaf rolling related genes, which involved in bulliform cells and cuticle development such as OsZHD1, OsLBD3-7, RFS, ACL1, CFL1, SND1, OsCESA5 and OsCESA6 were up or down regulated in the srl1-KO. Conclusions SRL1 might control leaf rolling by regulating a couple of genes that affecting cytological architecture of leaf cells such as bulliforms and cuticle of leaves.


Author(s):  
Xingzhe Yang ◽  
Feng Li ◽  
Jie Ma ◽  
Yan Liu ◽  
Xuejiao Wang ◽  
...  

AbstractIn recent years, the incidence of fatigue has been increasing, and the effective prevention and treatment of fatigue has become an urgent problem. As a result, the genetic research of fatigue has become a hot spot. Transcriptome-level regulation is the key link in the gene regulatory network. The transcriptome includes messenger RNAs (mRNAs) and noncoding RNAs (ncRNAs). MRNAs are common research targets in gene expression profiling. Noncoding RNAs, including miRNAs, lncRNAs, circRNAs and so on, have been developed rapidly. Studies have shown that miRNAs are closely related to the occurrence and development of fatigue. MiRNAs can regulate the immune inflammatory reaction in the central nervous system (CNS), regulate the transmission of nerve impulses and gene expression, regulate brain development and brain function, and participate in the occurrence and development of fatigue by regulating mitochondrial function and energy metabolism. LncRNAs can regulate dopaminergic neurons to participate in the occurrence and development of fatigue. This has certain value in the diagnosis of chronic fatigue syndrome (CFS). CircRNAs can participate in the occurrence and development of fatigue by regulating the NF-κB pathway, TNF-α and IL-1β. The ceRNA hypothesis posits that in addition to the function of miRNAs in unidirectional regulation, mRNAs, lncRNAs and circRNAs can regulate gene expression by competitive binding with miRNAs, forming a ceRNA regulatory network with miRNAs. Therefore, we suggest that the miRNA-centered ceRNA regulatory network is closely related to fatigue. At present, there are few studies on fatigue-related ncRNA genes, and most of these limited studies are on miRNAs in ncRNAs. However, there are a few studies on the relationship between lncRNAs, cirRNAs and fatigue. Less research is available on the pathogenesis of fatigue based on the ceRNA regulatory network. Therefore, exploring the complex mechanism of fatigue based on the ceRNA regulatory network is of great significance. In this review, we summarize the relationship between miRNAs, lncRNAs and circRNAs in ncRNAs and fatigue, and focus on exploring the regulatory role of the miRNA-centered ceRNA regulatory network in the occurrence and development of fatigue, in order to gain a comprehensive, in-depth and new understanding of the essence of the fatigue gene regulatory network.


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