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Research article
Hu Huang
Corresponding Author
ORCiD: https://orcid.org/0000-0003-2843-0320
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Background Retinal degenerative diseases affect millions of people and represent the leading cause of vision loss around the world. Retinal degeneration has been attributed to a wide variety of causes, such as disruption of genes involved in phototransduction, biosynthesis, folding of the rhodopsin molecule, and the structural support of the retina. The molecular pathogenesis of the biological events in retinal degeneration is unclear; however, the molecular basis of the retinal pathological defect can be potentially determined by gene-expression profiling of the whole retina. In the present study, we analyzed the differential gene expression profile of the retina from a wild-type zebrafish and phosphodiesterase 6c (pde6c) mutant. Results The datasets were downloaded from the Sequence Read Archive (SRA), and adaptors and unbiased bases were removed, and sequences were checked to ensure the quality. The reads were further aligned to the reference genome of zebrafish, and the gene expression was calculated. The differentially expressed genes (DEGs) were filtered based on the false discovery rate (FDR) (±4) and p-values (p < 0.001). We performed gene annotation (molecular function [MF], biological process [BP], cellular component [CC]), and determined the functional pathways Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway for the DEGs. Our result showed 216 upregulated and 3,527 downregulated genes between normal and pde6c mutant zebrafish. These DEGs are involved in various KEGG pathways, such as the phototransduction (12 genes), mRNA surveillance (17 genes), phagosome (25 genes), glycolysis/gluconeogenesis (15 genes), adrenergic signaling in cardiomyocytes (29 genes), ribosome (20 genes), the citrate cycle (TCA cycle; 8 genes), insulin signaling (24 genes), oxidative phosphorylation (20 genes), and RNA transport (22 genes) pathways. Many more of all the pathway genes were downregulated, while fewer were upregulated in the retina of mutant zebrafish. Conclusions Our data strongly indicate that, among these genes, the above-mentioned pathways’ genes as well as calcium-binding, neural damage, peptidase, immunological, and apoptosis proteins are mostly involved in the retinal and neural degeneration that cause abnormalities in photoreceptors or retinal pigment epithelium (RPE) cells.
Keywords
Pde6c, Zebrafish, Gene ontology, FastQC, Trinity, KEGG.
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CURRENT STATUS: Published
View the published article at BMC Genomics.
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On 31 Jan, 2020
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On 30 Jan, 2020
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Editorial decision: Minor revision
On 24 Jan, 2020
Editor assigned
On 23 Jan, 2020
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On 22 Jan, 2020
No comments provided
Editorial decision: Minor revision
On 08 Dec, 2019
Review #1 received
Received 04 Dec, 2019
Reviewers invited
Invitations sent on 28 Nov, 2019
Reviewer #1 agreed
On 28 Nov, 2019
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On 26 Nov, 2019
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On 25 Nov, 2019
Editor invited
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Editorial decision: Minor revision
On 06 Nov, 2019
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Received 25 Sep, 2019
Review #1 received
Received 17 Sep, 2019
Reviewers invited
Invitations sent on 12 Sep, 2019
Reviewer #1 agreed
On 12 Sep, 2019
Reviewer #2 agreed
On 12 Sep, 2019
Editor assigned
On 14 Aug, 2019
Submission checks complete
On 13 Aug, 2019
Editor invited
On 13 Aug, 2019
No comments provided
Editorial decision: Major revision
On 29 Jul, 2019
Review #2 received
Received 23 Jul, 2019
Reviewer #3 agreed
On 16 Jul, 2019
Review #1 received
Received 26 Jun, 2019
Reviewer #2 agreed
On 24 Jun, 2019
Reviewer #1 agreed
On 18 Jun, 2019
Reviewers invited
Invitations sent on 17 Jun, 2019
Editor assigned
On 10 Jun, 2019
Submission checks complete
On 07 Jun, 2019
Editor invited
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On 29 May, 2019
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Subject Areas
Epigenetics & Genomics
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A new preprint design is coming!
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See the published version of this preprint at BMC Genomics.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research article
Hu Huang
Corresponding Author
ORCiD: https://orcid.org/0000-0003-2843-0320
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
View the published article at BMC Genomics.
Version 5
Posted 30 Jan, 2020
No community comments so far
Editorial decision: Accept
On 31 Jan, 2020
Editor assigned
On 30 Jan, 2020
Submission checks complete
On 29 Jan, 2020
Editor invited
On 29 Jan, 2020
No comments provided
Editorial decision: Minor revision
On 24 Jan, 2020
Editor assigned
On 23 Jan, 2020
Submission checks complete
On 22 Jan, 2020
Editor invited
On 22 Jan, 2020
No comments provided
Editorial decision: Minor revision
On 08 Dec, 2019
Review #1 received
Received 04 Dec, 2019
Reviewers invited
Invitations sent on 28 Nov, 2019
Reviewer #1 agreed
On 28 Nov, 2019
Editor assigned
On 26 Nov, 2019
Submission checks complete
On 25 Nov, 2019
Editor invited
On 25 Nov, 2019
No comments provided
Editorial decision: Minor revision
On 06 Nov, 2019
Review #2 received
Received 25 Sep, 2019
Review #1 received
Received 17 Sep, 2019
Reviewers invited
Invitations sent on 12 Sep, 2019
Reviewer #1 agreed
On 12 Sep, 2019
Reviewer #2 agreed
On 12 Sep, 2019
Editor assigned
On 14 Aug, 2019
Submission checks complete
On 13 Aug, 2019
Editor invited
On 13 Aug, 2019
No comments provided
Editorial decision: Major revision
On 29 Jul, 2019
Review #2 received
Received 23 Jul, 2019
Reviewer #3 agreed
On 16 Jul, 2019
Review #1 received
Received 26 Jun, 2019
Reviewer #2 agreed
On 24 Jun, 2019
Reviewer #1 agreed
On 18 Jun, 2019
Reviewers invited
Invitations sent on 17 Jun, 2019
Editor assigned
On 10 Jun, 2019
Submission checks complete
On 07 Jun, 2019
Editor invited
On 07 Jun, 2019
First submitted
On 29 May, 2019
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Epigenetics & Genomics
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at BMC Genomics.
Background Retinal degenerative diseases affect millions of people and represent the leading cause of vision loss around the world. Retinal degeneration has been attributed to a wide variety of causes, such as disruption of genes involved in phototransduction, biosynthesis, folding of the rhodopsin molecule, and the structural support of the retina. The molecular pathogenesis of the biological events in retinal degeneration is unclear; however, the molecular basis of the retinal pathological defect can be potentially determined by gene-expression profiling of the whole retina. In the present study, we analyzed the differential gene expression profile of the retina from a wild-type zebrafish and phosphodiesterase 6c (pde6c) mutant. Results The datasets were downloaded from the Sequence Read Archive (SRA), and adaptors and unbiased bases were removed, and sequences were checked to ensure the quality. The reads were further aligned to the reference genome of zebrafish, and the gene expression was calculated. The differentially expressed genes (DEGs) were filtered based on the false discovery rate (FDR) (±4) and p-values (p < 0.001). We performed gene annotation (molecular function [MF], biological process [BP], cellular component [CC]), and determined the functional pathways Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway for the DEGs. Our result showed 216 upregulated and 3,527 downregulated genes between normal and pde6c mutant zebrafish. These DEGs are involved in various KEGG pathways, such as the phototransduction (12 genes), mRNA surveillance (17 genes), phagosome (25 genes), glycolysis/gluconeogenesis (15 genes), adrenergic signaling in cardiomyocytes (29 genes), ribosome (20 genes), the citrate cycle (TCA cycle; 8 genes), insulin signaling (24 genes), oxidative phosphorylation (20 genes), and RNA transport (22 genes) pathways. Many more of all the pathway genes were downregulated, while fewer were upregulated in the retina of mutant zebrafish. Conclusions Our data strongly indicate that, among these genes, the above-mentioned pathways’ genes as well as calcium-binding, neural damage, peptidase, immunological, and apoptosis proteins are mostly involved in the retinal and neural degeneration that cause abnormalities in photoreceptors or retinal pigment epithelium (RPE) cells.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
This is a list of supplementary files associated with this preprint. Click to download.
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