Zebrafish null mutants of Sept6 and Sept15 are viable but more susceptible to Shigella infection

• Published in: Cytoskeleton (Hoboken, N.J.) Vol. 80; no. 7-8; pp. 266 - 274
• Main Authors: Torraca, Vincenzo, Bielecka, Magdalena K, Gomes, Margarida C, Brokatzky, Dominik, Busch-Nentwich, Elisabeth M, Mostowy, Serge
• Format: Journal Article
• Language: English
• Published: United States Wiley Subscription Services, Inc 01.07.2023; John Wiley & Sons, Inc
• Subjects: Animal models; Animals; Cell division; Danio rerio; Dysentery, Bacillary - genetics; Genomes; GTP-Binding Proteins - genetics; GTP-Binding Proteins - metabolism; Infections; Mutants; Septin; Septins - genetics; Septins - metabolism; Shigella; Short Report; Zebrafish - genetics; Zebrafish - metabolism; zebrafish; cytoskeleton; null mutant; genetic compensation; Shigella; septins
• ISSN: 1949-3584; 1949-3592; 1949-3592
• DOI: 10.1002/cm.21750

Septins are evolutionarily conserved GTP-binding proteins known for their roles in cell division and host defence against Shigella infection. Although septin group members are viewed to function as hetero-oligomeric complexes, the role of individual septins within these complexes or in isolation is poorly understood. Decades of work using mouse models has shown that some septins (including SEPT7) are essential for animal development, while others (including SEPT6) are dispensable, suggesting that some septins may compensate for the absence of others. The zebrafish genome encodes 19 septin genes, representing the full complement of septin groups described in mice and humans. In this report, we characterise null mutants for zebrafish Sept6 (a member of the SEPT6 group) and Sept15 (a member of the SEPT7 group) and test their role in zebrafish development and host defence against Shigella infection. We show that null mutants for Sept6 and Sept15 are both viable, and that expression of other zebrafish septins are not significantly affected by their mutation. Consistent with previous reports using knockdown of Sept2, Sept7b, and Sept15, we show that Sept6 and Sept15 are required for host defence against Shigella infection. These results highlight Shigella infection of zebrafish as a powerful system to study the role of individual septins in vivo.