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Lymphatic Defects in Zebrafish sox18 Mutants Are Exacerbated by Perturbed VEGFC Signaling, While Masked by Elevated
Silvia Moleri1, Sara Mercurio2, Alex Pezzotta1
1Dipartimento di Bioscienze, Università degli Studi di Milano, Via Celoria 26, 20133 Milan, Italy.
Cells
|September 28, 2023
Summary
A novel zebrafish sox18 mutant reveals Sox7 can compensate for SOX18 loss in lymphatic development. This genetic interaction with Vegfc highlights Sox7
Area of Science:
- Developmental Biology
- Genetics
- Molecular Biology
Background:
- Primary lymphedema is linked to mutations in SOX18, VEGFC, and VEGFR3.
- SOX18 and COUP-TFII activate Prox1, a key regulator of lymphatic development.
- Previous studies suggested Sox18, Coup-tfII, and Prox1 involvement in zebrafish lymphatics.
Purpose of the Study:
- To characterize a novel zebrafish sox18 mutant allele (sa12315) with null activity.
- To investigate the role of SOX18 in lymphatic development and its interaction with other genes.
- To explore the compensatory mechanisms in zebrafish lymphatic development.
Main Methods:
- Generated and analyzed a novel zebrafish sox18 mutant allele (sa12315).
- Assessed lymphatic thoracic duct formation in sox18 mutants (zygotic and maternal-zygotic).
- Examined gene expression changes, specifically sox7, in sox18 mutants.
- Performed partial knockdown of vegfc in sox18 mutants to study gene interactions.
Main Results:
- The sox18 mutant (sa12315) exhibited milder lymphatic defects than morphants.
- Elevated expression of the related sox7 gene was observed in sox18 mutants.
- Sox7 appears to compensate for the loss of Sox18 function in lymphatic development.
- Partial vegfc knockdown exacerbated lymphatic defects in sox18 mutants, even in heterozygotes.
Conclusions:
- Sox7 can compensate for SOX18 loss-of-function in zebrafish lymphatic development.
- The genetic interaction between Sox18 and Vegfc is crucial for lymphatic development.
- The novel sox18 mutant provides a valuable tool for studying lymphatic disorders.
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