Paired fins in vertebrate evolution and ontogeny.

The origin of paired appendages became one of the most important adaptations of vertebrates, allowing them to lead active lifestyles and explore a wide range of ecological niches. The basic form of paired appendages in evolution is the fins of fishes. The problem of paired appendages has attracted the attention of researchers for more than 150 years. During this time, a number of theories have been proposed, mainly based on morphological data, two of which, the Balfour-Thacher-Mivart lateral fold theory and Gegenbaur's gill arch theory, have not lost their relevance. So far, however, none of the proposed ideas has been supported by decisive evidence. The study of the evolutionary history of the appearance and development of paired appendages lies at the intersection of several disciplines and involves the synthesis of paleontological, morphological, embryological, and genetic data. In this review, we attempt to summarize and discuss the results accumulated in these fields and to analyze the theories put forward regarding the prerequisites and mechanisms that gave rise to paired fins and limbs in vertebrates.

wnt10a is required for zebrafish median fin fold maintenance and adult unpaired fin metamorphosis.

BACKGROUND: Mutations of human WNT10A are associated with odonto-ectodermal dysplasia syndromes. Here, we present analyses of wnt10a loss-of-function mutants in the zebrafish. RESULTS: wnt10a mutant zebrafish embryos display impaired tooth development and a collapsing median fin fold (MFF). Rescue experiments show that wnt10a is essential for MFF maintenance both during embryogenesis and later metamorphosis. The MFF collapse could not be attributed to increased cell death or altered proliferation rates of MFF cell types. Rather, wnt10a mutants show reduced expression levels of dlx2a in distal-most MFF cells, followed by compromised expression of col1a1a and other extracellular matrix proteins encoding genes. Transmission electron microscopy analysis shows that although dermal MFF compartments of wnt10a mutants initially are of normal morphology, with regular collagenous actinotrichia, positioning of actinotrichia within the cleft of distal MFF cells becomes compromised, coinciding with actinotrichia shrinkage and MFF collapse. CONCLUSIONS: MFF collapse of wnt10a mutant zebrafish is likely caused by the loss of distal properties in the developing MFF, strikingly similar to the proposed molecular pathomechanisms underlying the teeth defects caused by the loss of Wnt10 in fish and mammals. In addition, it points to thus fur unknown mechanisms controlling the linear growth and stability of actinotrichia and their collagen fibrils.

Bone Morphogenetic Protein Signaling Restricts Proximodistal Extension of the Ventral Fin Fold.

Unpaired fins, which are the most ancient form of locomotory appendages in chordates, had emerged at least 500 million years ago. While it has been suggested that unpaired fins and paired fins share structural similarities, cellular and molecular mechanisms that regulate the outgrowth of the former have not been fully elucidated yet. Using the ventral fin fold in zebrafish as a model, here, we investigate how the outgrowth of the unpaired fin is modulated. We show that Bone Morphogenetic Protein (BMP) signaling restricts extension of the ventral fin fold along the proximodistal axis by modulating diverse aspects of cellular behaviors. We find that lack of BMP signaling, either caused by genetic or chemical manipulation, prolongs the proliferative capacity of epithelial cells and substantially increases the number of cells within the ventral fin fold. In addition, inhibition of BMP signaling attenuates the innate propensity of cell division along the anteroposterior axis and shifts the orientation of cell division toward the proximodistal axis. Moreover, abrogating BMP signaling appears to induce excessive distal migration of cells within the ventral fin fold, and therefore precipitates extension along the proximodistal axis. Taken together, our data suggest that BMP signaling restricts the outgrowth of the ventral fin fold during zebrafish development.

Fin-fold development in paddlefish and catshark and implications for the evolution of the autopod.

The evolutionary origin of the autopod involved a loss of the fin-fold and associated dermal skeleton with a concomitant elaboration of the distal endoskeleton to form a wrist and digits. Developmental studies, primarily from teleosts and amniotes, suggest a model for appendage evolution in which a delay in the AER-to-fin-fold conversion fuelled endoskeletal expansion by prolonging the function of AER-mediated regulatory networks. Here, we characterize aspects of paired fin development in the paddlefish Polyodon spathula (a non-teleost actinopterygian) and catshark Scyliorhinus canicula (chondrichthyan) to explore aspects of this model in a broader phylogenetic context. Our data demonstrate that in basal gnathostomes, the autopod marker HoxA13 co-localizes with the dermoskeleton component And1 to mark the position of the fin-fold, supporting recent work demonstrating a role for HoxA13 in zebrafish fin ray development. Additionally, we show that in paddlefish, the proximal fin and fin-fold mesenchyme share a common mesodermal origin, and that components of the Shh/LIM/Gremlin/Fgf transcriptional network critical to limb bud outgrowth and patterning are expressed in the fin-fold with a profile similar to that of tetrapods. Together these data draw contrast with hypotheses of AER heterochrony and suggest that limb-specific morphologies arose through evolutionary changes in the differentiation outcome of conserved early distal patterning compartments.

Transient inflammatory response mediated by interleukin-1ß is required for proper regeneration in zebrafish fin fold.

Cellular responses to injury are crucial for complete tissue regeneration, but their underlying processes remain incompletely elucidated. We have previously reported that myeloid-defective zebrafish mutants display apoptosis of regenerative cells during fin fold regeneration. Here, we found that the apoptosis phenotype is induced by prolonged expression of interleukin 1 beta (il1b). Myeloid cells are considered to be the principal source of Il1b, but we show that epithelial cells express il1b in response to tissue injury and initiate the inflammatory response, and that its resolution by macrophages is necessary for survival of regenerative cells. We further show that Il1b plays an essential role in normal fin fold regeneration by regulating expression of regeneration-induced genes. Our study reveals that proper levels of Il1b signaling and tissue inflammation, which are tuned by macrophages, play a crucial role in tissue regeneration.

Fish larvae exploit edge vortices along their dorsal and ventral fin folds to propel themselves.

Larvae of bony fish swim in the intermediate Reynolds number (Re) regime, using body- and caudal-fin undulation to propel themselves. They share a median fin fold that transforms into separate median fins as they grow into juveniles. The fin fold was suggested to be an adaption for locomotion in the intermediate Reynolds regime, but its fluid-dynamic role is still enigmatic. Using three-dimensional fluid-dynamic computations, we quantified the swimming trajectory from body-shape changes during cyclic swimming of larval fish. We predicted unsteady vortices around the upper and lower edges of the fin fold, and identified similar vortices around real larvae with particle image velocimetry. We show that thrust contributions on the body peak adjacent to the upper and lower edges of the fin fold where large left-right pressure differences occur in concert with the periodical generation and shedding of edge vortices. The fin fold enhances effective flow separation and drag-based thrust. Along the body, net thrust is generated in multiple zones posterior to the centre of mass. Counterfactual simulations exploring the effect of having a fin fold across a range of Reynolds numbers show that the fin fold helps larvae achieve high swimming speeds, yet requires high power. We conclude that propulsion in larval fish partly relies on unsteady high-intensity vortices along the upper and lower edges of the fin fold, providing a functional explanation for the omnipresence of the fin fold in bony-fish larvae.

A diffusible signal derived from hematopoietic cells supports the survival and proliferation of regenerative cells during zebrafish fin fold regeneration.

Multicellular organisms maintain body integrity by constantly regenerating tissues throughout their lives; however, the overall mechanism for regulating regeneration remains an open question. Studies of limb and fin regeneration in teleost fish and urodeles have shown the involvement of a number of locally activated signals at the wounded site during regeneration. Here, we demonstrate that a diffusible signal from a distance also play an essential role for regeneration. Among a number of zebrafish mutants, we found that the zebrafish cloche (clo) and tal1 mutants, which lack most hematopoietic tissues, displayed a unique regeneration defect accompanying apoptosis in primed regenerative tissue. Our analyses of the mutants showed that the cells in the primed regenerative tissue are susceptible to apoptosis, but their survival is normally supported by the presence of hematopoietic tissues, mainly the myeloid cells. We further showed that a diffusible factor in the wild-type body fluid mediates this signal. Thus, our study revealed a novel mechanism that the hematopoietic tissues regulate tissue regeneration through a diffusible signal.

Canonical Wnt signalling regulates epithelial patterning by modulating levels of laminins in zebrafish appendages.

The patterning and morphogenesis of body appendages - such as limbs and fins - is orchestrated by the activities of several developmental pathways. Wnt signalling is essential for the induction of limbs. However, it is unclear whether a canonical Wnt signalling gradient exists and regulates the patterning of epithelium in vertebrate appendages. Using an evolutionarily old appendage - the median fin in zebrafish - as a model, we show that the fin epithelium exhibits graded changes in cellular morphology along the proximo-distal axis. This epithelial pattern is strictly correlated with the gradient of canonical Wnt signalling activity. By combining genetic analyses with cellular imaging, we show that canonical Wnt signalling regulates epithelial cell morphology by modulating the levels of laminins, which are extracellular matrix components. We have unravelled a hitherto unknown mechanism involved in epithelial patterning, which is also conserved in the pectoral fins - evolutionarily recent appendages that are homologous to tetrapod limbs.

The effect of rearing temperature in larval development of pejerrey, Odontesthes bonariensis: morphological indicators of development

It is well known that in pejerrey water temperature not only affects growth rates but also directs the sexual differentiation process. This fact rise the question of how different the development of pejerrey larvae of the same age is when reared at different temperatures. A description of developmental stages for the embryonic and larval periods of the pejerrey, Odontesthes bonariensis, and the influence of rearing temperature on larval development are presented. Then, larval development was studied at three rearing temperatures, and changes in general morphology, fin morphology, and caudal fin structure have been taken into consideration within the thermal range involved in the temperature sex determination of this species. Fin fold reabsorption, caudal fin formation, and body shape were selected to follow the events leading to the acquisition of the juvenile morphology. The juvenile phenotype was defined when the fin fold was reabsorpted and the caudal fin acquired its definitive homocercal structure. The moment at which the juvenile phenotype was achieved, was evaluated in relation to larval age, size and, shape. The size resulted as the best indicator of development in pejerrey.

A temperatura da água não afeta apenas as taxas de crescimento no peixe-rei, mas também direciona o processo de diferenciação sexual. Este fato levanta o questionamento de quão diferente é o desenvolvimento de larvas do peixe-rei da mesma idade quando criadas em temperaturas diferentes. Este trabalho teve como objetivo apresentar uma descrição do de desenvolvimento de embriões e larvas do peixe-rei, Odontesthes bonariensis, e a influência da temperatura de criação no desenvolvimento das larvas. Neste trabalho, o desenvolvimento das larvas foi estudado em três temperaturas diferentes de cultivo. Foram consideradas as alterações ocorridas na morfologia geral, assim como na morfologia e na estrutura da nadadeira caudal dentro da variação termal da temperatura de determinação sexual desta espécie. A taxa de reabsorção da membrana embrionária, a formação da cauda e o formato do corpo foram selecionados para acompanhar os eventos que levam à aquisição da morfologia juvenil. O fenótipo juvenil foi definido quando a nadadeira caudal foi reabsorvida e a cauda adquiriu a estrutura homocerca. O momento no qual o fenótipo juvenil foi atingido, foi avaliado quanto à idade, tamanho e formato da larva, sendo que o tamanho resultou no melhor indicador do desenvolvimento do peixe-rei.