The Skt gene, required for anorectal development, is a candidate for a molecular marker of the cloacal plate
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Hiroko Suda1, Kwang-Jong Lee, Kei Semba
1Division of Developmental Genetics, Center for Animal Resources and Development, Institute of Resource Development and Analysis, Kumamoto University, 2-2-1 Honjo, Kumamoto, Japan.
Background And Aims:
It has been reported that a dorsal cloacal plate defect is associated with anorectal malformations (ARMs); however, there has been very little information reported about the developmental mechanisms involved with cloacal plate formation. Danforth's short tail (Sd) mutant mice show ARMs. In our previous study, the co-presence of Skt ( Gt ) mutation, in which Skt gene is disrupted by the gene-trap vector (p-U8), increased the incidence of ARMs in Sd mutant to 100%. Our aims in this study are determining the Skt expression around the cloaca during the anorectal development and demonstrating the role of Skt gene in ARMs.
Methods:
Embryos, normal controls [+Skt ( Gt )/+Skt ( Gt )] and ARMs models [Sd Skt ( Gt )/+Skt ( Gt )], from embryonic day (E) 9.5 to E12.5, were evaluated with X-gal staining.
Results:
In control embryos, Skt expression was detected both in the endoderm and ectoderm of the cloacal plate from E9.5 onward. At E12.5, Skt expression was also detected in the mesenchyme neighboring the dorsal cloacal plates. In [Sd Skt ( Gt )/+Skt ( Gt )] mutant embryos, the cloacal plates failed to extend proximodistally and, consequently, the dorsal part of cloacal plate was defective at E11.5. Skt expressing cells were detected in the shortened cloacal plate and in the thickened mesenchyme dorsal to it.
Conclusions:
We showed the spatial and temporal expression of Skt gene in the cloacal plate formation. This gene could be a marker for the cloacal plate during the anorectal development. Furthermore, Skt was considered to be associated with the embryogenesis of ARMs.
Insights
The Skt gene is crucial for cloacal plate formation during anorectal development. Its disruption is linked to anorectal malformations (ARMs) in mice, suggesting Skt as a potential marker for ARMs.
Area of Science:
- Developmental Biology
- Genetics
- Embryology
Background:
- Dorsal cloacal plate defects are associated with anorectal malformations (ARMs).
- Limited information exists on cloacal plate formation mechanisms.
- Danforth's short tail (Sd) mutant mice exhibit ARMs, with a 100% incidence when combined with a Skt (Gt) mutation.
Purpose of the Study:
- To determine the spatial and temporal expression of the Skt gene during anorectal development.
- To elucidate the role of the Skt gene in the embryogenesis of ARMs.
Main Methods:
- Analysis of normal control embryos [+Skt (Gt)/+Skt (Gt)] and ARM models [Sd Skt (Gt)/+Skt (Gt)] from embryonic day (E) 9.5 to E12.5.
- Evaluation using X-gal staining to detect Skt expression.
Main Results:
- Skt expression was observed in the cloacal plate's endoderm and ectoderm from E9.5 in controls.
- In mutant embryos, cloacal plates showed proximodistal shortening and dorsal defects by E11.5.
- Skt-expressing cells were present in the shortened cloacal plate and surrounding mesenchyme of mutants.
Conclusions:
- The Skt gene exhibits specific spatial and temporal expression patterns during cloacal plate formation.
- Skt gene expression can serve as a marker for the cloacal plate in anorectal development.
- The Skt gene is implicated in the embryogenesis of anorectal malformations.
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