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Transposon insertion causes ctnnb2 transcript instability that results in the maternal effect zebrafish ichabod (ich)
Zsombor Varga1, Ferenc Kagan2, Shingo Maegawa3
1Department of Genetics, ELTE Eötvös Loránd University, Budapest, Hungary.
Summary
The ichabod mutation in zebrafish causes ventralized embryos by disrupting Wnt signaling. A transposon insertion in the ctnnb2 gene reduces its transcript stability, explaining the developmental defect.
Area of Science:
- Developmental Biology
- Genetics
- Molecular Biology
Background:
- The maternal-effect mutation ichabod (ich) in zebrafish leads to ventralized embryos.
- This phenotype is linked to impaired dorsal canonical Wnt-signaling pathway induction.
- Previous research suggested reduced ctnnb2 transcript levels, but the causative mutation was unknown.
Purpose of the Study:
- To identify the molecular basis of the ichabod mutation.
- To investigate the role of transposon activity in zebrafish development.
- To understand maternal transcript regulation of ctnnb2.
Main Methods:
- Long-read sequencing to identify the causative mutation.
- Reporter assays to assess mRNA stability.
- Genome-wide mapping of transposon activity.
Main Results:
- The ich phenotype results from a CMC-Enhancer/Suppressor-mutator (CMC-EnSpm) transposon insertion in the 3'UTR of the ctnnb2 gene.
- This transposon insertion significantly reduces ctnnb2 mRNA stability.
- Ongoing transposition activity of CMC-EnSpm was detected in zebrafish.
Conclusions:
- The molecular cause of the ich mutation is an endogenous transposon insertion affecting maternal transcript stability.
- Endogenous transposons possess significant mutagenic potential in zebrafish.
- Maternal regulation of transcript stability plays a critical role in early zebrafish development.
