PUBLICATION

Zebrafish sox2 Is Required for the Swim Bladder Inflation by Controlling the Swim-Up Behavior

Authors
Cao, S., Dong, Z., Dong, X., Jia, W., Zhou, F., Zhao, Q.
ID
ZDB-PUB-230217-37
Date
2023
Source
Zebrafish   20: 101810-18 (Journal)
Registered Authors
Zhao, Qingshun
Keywords
motoneuron, sox2, swim bladder, zebrafish
MeSH Terms
  • Animals
  • Embryo, Nonmammalian/physiology
  • Locomotion
  • Organogenesis
  • SOX Transcription Factors*/genetics
  • Urinary Bladder
  • Zebrafish*/genetics
  • Zebrafish Proteins*/genetics
PubMed
36795618 Full text @ Zebrafish
Abstract
The swim bladder functions to maintain the fish balance at a certain position under water. Although the motoneuron-dependent swim-up behavior is important for swim bladder inflation, the underlying molecular mechanism remains largely unknown. We generated a sox2 KO zebrafish using TALEN and found that the posterior chamber of the swim bladder was uninflated. The tail flick and the swim-up behavior were absent in the mutant zebrafish embryos and the behavior could not be accomplished. As the tail flick behavior is absent, the mutant larvae therefore cannot reach the water surface to gulp air, ultimately leading to the uninflation of the swim bladder. To understand the mechanism underlying the swim-up defects, we crossed the sox2 null allele in the background of Tg(huc:eGFP) and Tg(hb9:GFP). The deficiency of sox2 in zebrafish resulted in abnormal motoneuron axons in the regions of trunk, tail, and swim bladder. To identify the downstream target gene of sox2 to control the motor neuron development, we performed RNA sequencing on the transcriber of mutant embryos versus wild type embryos and found that the axon guidance pathway was abnormal in the mutant embryos. RT-PCR demonstrated that the expression of sema3bl, ntn1b, and robo2 were decreased in the mutants.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping