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Updated: Oct 8, 2025
Isolation and RNA Extraction of Neurons, Macrophages and Microglia from Larval Zebrafish Brains
Published on: April 27, 2018
Transcriptome analysis of the early stage ifnlr1-mutant zebrafish indicates the immune response to auditory
Wei-Qian Wang1, Shi-Wei Qiu2, Sha-Sha Huang2
1College of Otolaryngology Head and Neck Surgery, Chinese PLA General Hospital, National Clinical Research Center for Otolaryngologic Diseases, State Key Lab of Hearing Science, Ministry of Education, China, Beijing Key Lab of Hearing Impairment Prevention and Treatment, Medical School of Chinese PLA, 28 Fuxing Road, Beijing, 100853, China; Department of Otolaryngology, PLA Rocket Force Characteristic Medical Center, 16# XinWai Da Jie, Beijing, 100088, China.
Background:
IFNLR1 has been recently identified to be related to autosomal dominant nonsyndromic sensorineural hearing loss (ADNSHL). It is reported to be expressed in the inner ear of mice and the lateral line of zebrafish. However, it remains unclear how defects in this gene lead to hearing loss.
Objectives:
To elucidate the global gene expression changes in zebrafish when the expression of ifnlr1 is downregulated.
Methods:
Transcriptome analysis was performed on ifnlr1 morpholino knockdown zebrafish and the control zebrafish using RNA-seq technology.
Results:
The results show that 262 differentially expressed genes (DEGs) were up-regulated while 146 DEGs were down-regulated in the E4I4-Mo zebrafish larvae compared to the control-Mo. Six pathways were significantly enriched, including steroid biosynthesis pathway, adipocytokine signaling pathway, cytokine-cytokine receptor interaction pathway, p53 signaling pathway, AGE-RAGE signaling pathway in diabetic complications, and terpenoid backbone biosynthesis pathway. Among them, three pathways (steroid biosynthesis pathway, cytokine-cytokine receptor interaction pathway and p53 signaling pathway) are immune-associated.
Conclusions:
The transcriptome analysis results contribute to the groundwork for future research on the pathogenesis of IFNLR1-associated hearing loss.
