PUBLICATION

Genome-wide identification of novel long non-coding RNAs and their possible roles in hypoxic zebrafish brain

Authors
Banerjee, B., Koner, D., Karasik, D., Saha, N.
ID
ZDB-PUB-201203-9
Date
2020
Source
Genomics   113(1 Pt 1): 29-43 (Journal)
Registered Authors
Karasik, David
Keywords
Alzheimer's disease, Brain regions, Hypoxia, Long non-coding RNAs, Zebrafish
Datasets
GEO:GSE153687
MeSH Terms
  • Animals
  • Brain/metabolism*
  • Hypoxia/genetics*
  • Hypoxia/metabolism
  • Metabolic Networks and Pathways/genetics
  • RNA, Long Noncoding/genetics*
  • RNA, Long Noncoding/metabolism
  • Zebrafish
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed
33264657 Full text @ Genomics
Abstract
Long non-coding RNAs (lncRNAs) are the master regulators of numerous biological processes. Hypoxia causes oxidative stress with severe and detrimental effects on brain function and acts as a critical initiating factor in the pathogenesis of Alzheimer's disease (AD). From the RNA-Seq in the forebrain (Fb), midbrain (Mb), and hindbrain (Hb) regions of hypoxic and normoxic zebrafish, we identified novel lncRNAs, whose potential cis targets showed involvement in neuronal development and differentiation pathways. Under hypoxia, several lncRNAs and mRNAs were differentially expressed. Co-expression studies indicated that the Fb and Hb regions' potential lncRNA target genes were involved in the AD pathogenesis. In contrast, those in Mb (cry1b, per1a, cipca) was responsible for regulating circadian rhythm. We identified specific lncRNAs present in the syntenic regions between zebrafish and humans, possibly functionally conserved. We thus identified several conserved lncRNAs as the probable regulators of AD genes (adrb3b, cav1, stat3, bace2, apoeb, psen1, s100b).
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping