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

Area of Science:

• Developmental Biology
• Neuroscience
• Genetics

Background:

• The swim bladder is essential for fish buoyancy and balance.
• Swim-up behavior, driven by motoneurons, is critical for swim bladder inflation.
• The molecular mechanisms regulating swim-up behavior and swim bladder inflation are not fully understood.

Purpose of the Study:

• To investigate the role of SOX2 in zebrafish swim bladder inflation and associated behaviors.
• To elucidate the molecular mechanisms by which SOX2 influences motoneuron development and axon guidance.

Main Methods:

• Generation of SOX2 knockout (KO) zebrafish using TALEN.
• Analysis of swim bladder inflation and swim-up behavior in mutant embryos.
• Crossing SOX2 KO zebrafish with Tg(huc:eGFP) and Tg(hb9:GFP) reporter lines.
• RNA sequencing to identify downstream target genes.
• RT-PCR to validate gene expression changes.

Main Results:

• SOX2 KO zebrafish displayed uninflated posterior swim bladders.
• Mutant embryos lacked tail flick and swim-up behaviors, preventing air gulping.
• SOX2 deficiency led to abnormal motoneuron axon development in trunk, tail, and swim bladder regions.
• RNA sequencing revealed defects in the axon guidance pathway.
• Expression of axon guidance molecules (sema3bl, ntn1b, robo2) was reduced in SOX2 mutants.

Conclusions:

• SOX2 is essential for normal swim bladder inflation in zebrafish.
• SOX2 plays a critical role in motoneuron development and axon guidance.
• Defects in SOX2-mediated axon guidance disrupt swim-up behavior, leading to swim bladder inflation failure.