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Characterization of Actinodin 1 and Actinodin 2 Loss-of-function Mutations in Zebrafish

Zebrafish (Danio rerio) are ray-finned fish of the teleost class, whose fins consist of an
exoskeletal domain and an endoskeletal domain. The exoskeletal domain of the fins contains
the fin rays and originate from embryonic fin folds that elongate as the fins are growing. The
elongation of the fin fold is supported by two parallel sets of rigid fibrils oriented along the
proximal-distal axis, called actinotrichia. Actinotrichia fibrils are composed of two primary
components, a collagenous component and actinodin proteins. The actinodin proteins are
encoded for by the actinodin (and) family of genes which are found in the genomes of finned
fish while absent in limbed tetrapods. CRISPR/Cas9 was used to create loss-of-function
deletions in the and1 and and2 genes, resulting in the absence of actinotrichia in the zebrafish
double mutants. We hypothesised that the loss of actinotrichia during zebrafish development
would result in developmental defects leading to fin ray defects in the adult zebrafish. The
and1/2 mutants that lack actinotrichia presented with fin fold and cell migration defects during
development that persisted into adulthood and resulted in shorter fins, disturbed fin ray
patterning, and a decrease in ray number. In addition, an unexpected fusion between the
hypurals of the caudal fin endoskeleton revealed an additional function of the actinotrichia
fibrils in caudal fin endoskeletal patterning. During zebrafish development, actinotrichia fibrils
play a vital role in ensuring normal fin development, normal patterning and formation of the
fin rays, and the normal development of the caudal fin endoskeleton.

Identiferoai:union.ndltd.org:uottawa.ca/oai:ruor.uottawa.ca:10393/45825
Date11 January 2024
CreatorsBaird, Connor
ContributorsAkimenko, Marie-Andree
PublisherUniversité d'Ottawa / University of Ottawa
Source SetsUniversité d’Ottawa
LanguageEnglish
Detected LanguageEnglish
TypeThesis
Formatapplication/pdf

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