Comparative transcriptome analysis of papilla and skin in the sea cucumber, Apostichopus japonicus

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Abstract

Papilla and skin are two important organs of the sea cucumber. Both tissues have ectodermic origin, but they are morphologically and functionally very different. In the present study, we performed comparative transcriptome analysis of the papilla and skin from the sea cucumber ( Apostichopus japonicus) in order to identify and characterize gene expression profiles by using RNA-Seq technology. We generated 30.6 and 36.4 million clean reads from the papilla and skin and de novo assembled in 156,501 transcripts. The Gene Ontology (GO) analysis indicated that cell part, metabolic process and catalytic activity were the most abundant GO category in cell component, biological process and molecular funcation, respectively. Comparative transcriptome analysis between the papilla and skin allowed the identification of 1,059 differentially expressed genes, of which 739 genes were expressed at higher levels in papilla, while 320 were expressed at higher levels in skin. In addition, 236 differentially expressed unigenes were not annotated with any database, 160 of which were apparently expressed at higher levels in papilla, 76 were expressed at higher levels in skin. We identified a total of 288 papilla-specific genes, 171 skin-specific genes and 600 co-expressed genes. Also, 40 genes in papilla-specific were not annotated with any database, 2 in skin-specific. Development-related genes were also enriched, such as fibroblast growth factor, transforming growth factor-β, collagen-α2 and Integrin-α2, which may be related to the formation of the papilla and skin in sea cucumber. Further pathway analysis identified ten KEGG pathways that were differently enriched between the papilla and skin. The findings on expression profiles between two key organs of the sea cucumber should be valuable to reveal molecular mechanisms involved in the development of organs that are related but with morphological differences in the sea cucumber.

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Tissue stiffness, latent TGF-beta1 activation, and mechanical signal transduction: implications for the pathogenesis and treatment of fibrosis.

Boris Hinz (2009)

Tissue stiffening is a predominant feature of fibrosis and it obstructs organs whose mechanical properties are important for their function, such as the heart, lung, skin, and vessels. Stiff scar tissue further modulates the character of the healthy residing cells by driving the differentiation of a variety of precursor cells into fibrogenic myofibroblasts. This mechanical cue for myofibroblast differentiation establishes a vicious cycle because the excessive extracellular matrix-secreting and remodeling activities of myofibroblasts are cause and effect of further connective tissue contracture and stiffening. The second pivotal factor inducing myofibroblast development is transforming growth factor-beta1. Recent findings suggest that transforming growth factor-beta1 activity is partly controlled by myofibroblast contractile forces and tissue stiffness. This discovery opens new paths to prevent progression of fibrosis by specifically interfering with the stress perception and transmission mechanisms of the myofibroblast.

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Targeted disruption of Fgf8 causes failure of cell migration in the gastrulating mouse embryo.

X. Sun, E. Meyers, M Lewandoski … (1999)

Fgf8 and Fgf4 encode FGF family members that are coexpressed in the primitive streak of the gastrulating mouse embryo. We have analyzed the phenotype of Fgf8(-/-) embryos and discovered that they fail to express Fgf4 in the streak. In the absence of both FGF8 and FGF4, epiblast cells move into the streak and undergo an epithelial-to-mesenchymal transition, but most cells then fail to move away from the streak. As a consequence, no embryonic mesoderm- or endoderm-derived tissues develop, although extraembryonic tissues form. Patterning of the prospective neuroectoderm is greatly perturbed in the mutant embryos. Anterior neuroectoderm markers are widely expressed, at least in part because the anterior visceral endoderm, which provides signals that regulate their expression, is not displaced proximally in the absence of definitive endoderm. Posterior neuroectoderm markers are not expressed, presumably because there is neither mesendoderm underlying the prospective neuroectoderm nor a morphologically normal node to provide the inductive signals necessary for their expression. This study identifies Fgf8 as a gene essential for gastrulation and shows that signaling via FGF8 and/or FGF4 is required for cell migration away from the primitive streak.

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Genetics of keloid scarring.

Barbara Shih, Ardeshir Bayat (2010)

Keloid scarring, also known as keloid disease (KD), is a common, abnormally raised fibroproliferative cutaneous lesion that can occur following even minor skin trauma. The aetiopathogenesis of KD has remained an enigma todate compounded by an ill-defined clinical management. There is strong evidence suggesting a genetic susceptibility in individuals affected by KD, including familial heritability, common occurrence in twins and high prevalence in certain ethnic populations. This review aims to address the genetic aspects of KD that have been described in present literature that include inheritance patterns, linkage studies, case-control association studies, whole genome gene expression microarray studies and gene pathways that were significant in KD. In addition to our clinical and scientific background in KD, we used search engines, Scopus, Scirus and PubMed, which searched for key terms covering various genetic aspects of KD. Additionally, genes reported in seven whole genome gene expression microarray studies were separately compared in detail. Our findings indicate a varied inheritance pattern in KD (predominantly autosomal dominant), linkage loci (chromosomes 2q23 and 7p11), several human leukocyte antigen (HLA) alleles (HLA-DRB1*15, HLA-DQA1*0104, DQ-B1*0501 and DQB1*0503), negative candidate gene case-control association studies and at least 25 dysregulated genes reported in multiple microarray studies. The major pathways reportedly proposed to be involved in KD include apoptosis, mitogen-activated protein kinase, transforming growth factor-beta, interleukin-6 and plasminogen activator inhibitor-1. In summary, involvement of more than one gene is likely to be responsible for susceptibility to KD. A better understanding of the genes involved in KD may potentially lead to the development of more effective diagnostic, therapeutic and prognostic measures.

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Author and article information

Contributors

Xiuli Wang

Journal

Journal ID (nlm-ta): PeerJ

Journal ID (iso-abbrev): PeerJ

Journal ID (pmc): PeerJ

Journal ID (publisher-id): PeerJ

Title: PeerJ

Publisher: PeerJ Inc. (San Francisco, USA )

ISSN (Electronic): 2167-8359

Publication date (Electronic): 7 March 2016

Publication date Collection: 2016

Volume: 4

Electronic Location Identifier: e1779

Affiliations

[1 ]Key Laboratory of Mariculture & Stock Enhancement in North China’s Sea, Ministry of Agriculture, Dalian Ocean University , Dalian, China

[2 ]College of Fisheries and Life Science, Dalian Ocean University , Dalian, China

[3 ]The Fish Molecular Genetics and Biotechnology Laboratory, Aquatic Genomics Unit, School of Fisheries, Aquaculture and Aquatic Sciences and Program of Cell and Molecular Biosciences, Auburn University , Auburn, Alabama, United States

Article

Publisher ID: 1779

DOI: 10.7717/peerj.1779

PMC ID: 4793329

PubMed ID: 26989617

SO-VID: bea13f7c-2df2-45f2-9a3f-4467313cd0a0

License:

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ) and either DOI or URL of the article must be cited.

History

Date received : 12 November 2015

Date accepted : 17 February 2016

Funding

Funded by: State 863 High-Technology R & D Project of China

Award ID: 2012AA10A412

Funded by: Program for Liaoning Excellent Talents in University, China

Award ID: LR2014022

This project was supported by the State 863 High-Technology R & D Project of China (No. 2012AA10A412) and the Program for Liaoning Excellent Talents in University, China (No. LR2014022). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Comparative transcriptome analysis of papilla and skin in the sea cucumber, Apostichopus japonicus

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Most cited references 53

Tissue stiffness, latent TGF-beta1 activation, and mechanical signal transduction: implications for the pathogenesis and treatment of fibrosis.

Targeted disruption of Fgf8 causes failure of cell migration in the gastrulating mouse embryo.

Genetics of keloid scarring.

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