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The Biology of Sea Turtles, Vol. II
(Figure 5.3). Corpora lutea act as steroid secretory glands, releasing progesterone
in response to increased luteinizing hormone (Wibbels and Owens, unpublished
data). Increased progesterone is thought to stimulate albumin production in postovulatory females (Owens, 1980; Owens and Morris, 1985). Corpora lutea regress
during the nesting season such that at the end of the nesting season different size
classes of corpora lutea may be evident on the surface of the ovary (Owens, 1980;
Limpus, 1985) (Figure 5.3) Within a few months of the completion of the nesting
season, healing corpora lutea are typically disk shaped. These scars further regress,
and in females that have bred in the last season (i.e., <1 year ago), they are approximately 0.5 cm in diameter (termed corpora albicantia). Thereafter, they regress to
small (approximately 0.1–0.2 cm) permanent scars on the ovary. Their presence
indicates that the female has ovulated and presumably bred in a previous year
(Limpus, 1985; 1992).
5.5.3 VITELLOGENESIS
Vitellogenesis is the process through which protein and lipid is progressively stored
in the growing oocytes of oviparous animals, making up the yolk of the mature egg
(Guraya, 1989). The process is remarkably similar in all reptiles studied to date
(Guraya, 1989). However, little data are available on the physiological and biochemical processes that underlie vitellogenesis in sea turtles.
Vitellogenin (VTG), the main protein involved in vitellogenesis, is a relatively
large (205 kDa) protein synthesized in the liver and transported to the ovary in
plasma as part of a lipoprotein complex (Heck et al., 1997). As such, VTG carries
lipid (predominantly triglyceride) to the growing oocytes. Estrogen production by
the ovarian follicles appears to be the principal stimulus for the onset of VTG
production in turtles (Ho, 1987) and increased estrogen has been linked to VTG
secretion in L. kempii (Heck et al., 1997). Subsequently, Rostal et al. (1998) used
polyacrylamide assays to monitor the presence or absence of VTG in annually
breeding L. kempii. The protein band was visible in the postbreeding period persisting
through until courtship around 7 months later (Rostal et al., 1998). More recently,
Vargas (2000) has developed an enzyme-linked immunosorbent assay (ELISA) for
sea turtle VTG in L. kempii using primary antibody derived from Trachemys scripta.
This antibody has also been successfully tested in C. mydas using western blots
(Hamann, unpublished data).
As yet, no research with sea turtles has focused on VTG receptors or patterns
of synthesis in relation to oocyte growth. An understanding of these stages is
important because they mediate key steps in oocyte maturation. It appears that in
both birds and fish the uptake of yolk precursors including VTG is controlled by a
95-kDa protein receptor (George et al., 1987; Bujo et al., 1994; Davail et al., 1998).
These receptors are presumed to lie in the plasma membrane of the growing oocyte,
and their production is thought to precede yolk deposition. Moreover, they function
as transport receptors for lipoproteins and regulatory protein for lipid deposition
(Barber et al., 1991). A detailed understanding of VTG production, mobilization,
and the biochemistry of vitellogenesis is needed for sea turtles.
1123 book.book Page 144 Thursday, November 14, 2002 11:50 AM
The Biology of Sea Turtles, Vol. II
(Figure 5.3). Corpora lutea act as steroid secretory glands, releasing progesterone
in response to increased luteinizing hormone (Wibbels and Owens, unpublished
data). Increased progesterone is thought to stimulate albumin production in postovulatory females (Owens, 1980; Owens and Morris, 1985). Corpora lutea regress
during the nesting season such that at the end of the nesting season different size
classes of corpora lutea may be evident on the surface of the ovary (Owens, 1980;
Limpus, 1985) (Figure 5.3) Within a few months of the completion of the nesting
season, healing corpora lutea are typically disk shaped. These scars further regress,
and in females that have bred in the last season (i.e., <1 year ago), they are approximately 0.5 cm in diameter (termed corpora albicantia). Thereafter, they regress to
small (approximately 0.1–0.2 cm) permanent scars on the ovary. Their presence
indicates that the female has ovulated and presumably bred in a previous year
(Limpus, 1985; 1992).
5.5.3 VITELLOGENESIS
Vitellogenesis is the process through which protein and lipid is progressively stored
in the growing oocytes of oviparous animals, making up the yolk of the mature egg
(Guraya, 1989). The process is remarkably similar in all reptiles studied to date
(Guraya, 1989). However, little data are available on the physiological and biochemical processes that underlie vitellogenesis in sea turtles.
Vitellogenin (VTG), the main protein involved in vitellogenesis, is a relatively
large (205 kDa) protein synthesized in the liver and transported to the ovary in
plasma as part of a lipoprotein complex (Heck et al., 1997). As such, VTG carries
lipid (predominantly triglyceride) to the growing oocytes. Estrogen production by
the ovarian follicles appears to be the principal stimulus for the onset of VTG
production in turtles (Ho, 1987) and increased estrogen has been linked to VTG
secretion in L. kempii (Heck et al., 1997). Subsequently, Rostal et al. (1998) used
polyacrylamide assays to monitor the presence or absence of VTG in annually
breeding L. kempii. The protein band was visible in the postbreeding period persisting
through until courtship around 7 months later (Rostal et al., 1998). More recently,
Vargas (2000) has developed an enzyme-linked immunosorbent assay (ELISA) for
sea turtle VTG in L. kempii using primary antibody derived from Trachemys scripta.
This antibody has also been successfully tested in C. mydas using western blots
(Hamann, unpublished data).
As yet, no research with sea turtles has focused on VTG receptors or patterns
of synthesis in relation to oocyte growth. An understanding of these stages is
important because they mediate key steps in oocyte maturation. It appears that in
both birds and fish the uptake of yolk precursors including VTG is controlled by a
95-kDa protein receptor (George et al., 1987; Bujo et al., 1994; Davail et al., 1998).
These receptors are presumed to lie in the plasma membrane of the growing oocyte,
and their production is thought to precede yolk deposition. Moreover, they function
as transport receptors for lipoproteins and regulatory protein for lipid deposition
(Barber et al., 1991). A detailed understanding of VTG production, mobilization,
and the biochemistry of vitellogenesis is needed for sea turtles.
1123 book.book Page 144 Thursday, November 14, 2002 11:50 AM