Date Awarded


Document Type


Degree Name

Doctor of Philosophy (Ph.D.)


Virginia Institute of Marine Science


Incremental marks formed in the vertebral cartilage of most sharks, skates and rays are widely used as indicators of age in elasmobranch growth studies. Such information is essential for fisheries management, thus vertebral ageing has become an invaluable tool for investigating elasmobranch life history. Unfortunately, lack of information on the processes that regulate vertebral growth and mineralization limit efforts to correlate episodic stimuli with increment production. to address this research need, this dissertation investigated these processes through a detailed study on the vertebral cartilage of the clearnose skate, Raja eglanteria. Histologic observations indicated that changes in appositional cartilage growth are the catalyst for increment formation. Observations by scanning electron microscopy supported this conclusion by demonstrating that growth increments differ in the proportion of cells to mineralized matrix. In contrast, elemental analysis of vertebrae using energy-dispersive spectrophotometry demonstrated no change in mineral concentration between seasonal growth layers. This observation was advantageous, because uptake of the radiotracer &\sp{lcub}45{rcub}&Ca was ineffective in estimating the rates of vertebral calcification in captive R. eglanteria. Failure of this standard method appeared to reflect the free exchange of calcium between skeletal and serologic reservoirs. An in vitro method for measuring vertebral growth was developed using incorporation of &\sp{lcub}35{rcub}&S-sulfate as a marker for cartilage matrix synthesis. Certain conserved among elasmobranchs and higher vertebrates. The growth hormone-dependent serum factor insulin-like growth factor-I (IGF-I) increased vertebral matrix synthesis, suggesting an important role for this hormone in regulating elasmobranch skeletal growth. In contrast, corticosterone reduced &\sp{lcub}35{rcub}&S-sulfate uptake in vertebral cartilage, suggesting an inhibitory role for glucocorticosteroids in elasmobranch chondrogenesis. Calcitonin also inhibited vertebral matrix synthesis and, in vivo, may play some role in skeletal development or mineral homeostasis. Finally, nutritional status also appeared to influence vertebral growth in vitro, perhaps indirectly through effects on hormone production. In sum, this dissertation identified changes in cartilage growth as the impetus for vertebral growth zone production in R. eglanteria. Physiological mechanisms that likely regulate vertebral growth are described in this pioneer study on elasmobranch skeletal growth.



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