Vitellogenesis is the process of yolk protein formation in the oocytes during sexual maturation.[2] The term vitellogenesis comes from the Latin vitellus ("egg yolk"). Yolk proteins, such as Lipovitellin and Phosvitin, provides maturing oocytes with the metabolic energy required for development. Vitellogenins are the precursor proteins that lead to yolk protein accumulation in the oocyte. In vertebrates, estrogen and vitellogenin production have a positive correlation. When estrogen production in the ovary is increased via the activation of the hypothalmo-pituitary axis it leads to heightened vitellogenin production in the liver.[3] Vitellogenin production in the liver is the first step of vitellogenesis. Once Vitellogenins are released into the blood stream where they are then transported to the growing oocyte where they lead to yolk protein production. The transport of vitellogenins into the maturing oocyte is done via endocytosis mediated by a receptor which is a low-density lipoprotein receptor (LDLR). Yolk is a lipoprotein composed of proteins, phospholipids and neutral fats along with a small amount of glycogen. The yolk is synthesised in the liver of the female parent in soluble form. Through circulation it is transported to the follicle cells that surround the maturing ovum, and is deposited in the form of yolk platelets and granules in the ooplasm. The mitochondria and Golgi complex are said to bring about the conversion of the soluble form of yolk into insoluble granules or platelets.
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The two hormones responsible for vitellogenesis stimulation in insects are sesquiterpenoid juvenile hormone (JH) and ecdysteroid 20-hydroxyecdysone (E20). More recent studies are showing the importance of miRNA in vitellogenesis stimulation as well. The pathways that these hormones regulate is largely dependent on the evolutionary growth of the insect species. Together, JH, E20, and miRNA help synthesize vitellogenins within the fat body. JH uses a JH Methoprene tolerant /Taiman receptor complex that is regulated by JH to synthesis vitellogenins in the fat body.[4]
In cockroaches, for example, vitellogenesis can be stimulated by injection of juvenile hormone into immature females and mature males. In mosquitoes infected with Plasmodium, vitellogenesis may be manipulated by the parasites to reduce fecundity, thereby preserving nutrition in the infected individual.[5]
| I. Holoblastic (complete) cleavage | II. Meroblastic (incomplete) cleavage |
|---|---|
|
A. Isolecithal (sparse, evenly distributed yolk)
B. Mesolecithal (moderate vegetal yolk disposition)
|
A. Telolecithal (dense yolk throughout most of cell)
B. Centrolecithal (yolk in center of egg)
|
References
edit- ^ Greani S, Quilichini Y, Marchand B (2016). "Ultrastructural study of vitellogenesis and oogenesis of Crepidostomum metoecus (Digenea, Allocreadiidae), intestinal parasite of Salmo trutta (Pisces, Teleostei)". Parasite. 23: 47. doi:10.1051/parasite/2016057. PMC 5112763. PMID 27845028.
- ^ Wallace RA (1985). "Vitellogenesis and Oocyte Growth in Nonmammalian Vertebrates". In Browder LW (ed.). Oogenesis. Vol. 1. Boston, MA: Springer US. pp. 127–177. doi:10.1007/978-1-4615-6814-8_3. ISBN 978-1-4615-6816-2. PMID 3917200.
{{cite book}}:|journal=ignored (help) - ^ Ho SM (1987). "Endocrinology of Vitellogenesis". In Norris DG, Jones RE (eds.). Hormones and Reproduction in Fishes, Amphibians, and Reptiles. Boston, MA: Springer US. pp. 145–169. doi:10.1007/978-1-4613-1869-9_6. ISBN 978-1-4612-9042-1.
- ^ Wu Z, Yang L, He Q, Zhou S (2021-01-28). "Regulatory Mechanisms of Vitellogenesis in Insects". Frontiers in Cell and Developmental Biology. 8: 593613. doi:10.3389/fcell.2020.593613. PMC 7901893. PMID 33634094.
- ^ Hurd H (2003). "Manipulation of medically important insect vectors by their parasites". Annual Review of Entomology. 48 (1): 141–161. doi:10.1146/annurev.ento.48.091801.112722. PMID 12414739.
- ^ Gilbert SF (2003). Developmental biology (7th ed.). Sinauer. p. 214. ISBN 0-87893-258-5.
- ^ Kardong KV (2006). Vertebrates: Comparative Anatomy, Function, Evolution (4th ed.). McGraw-Hill. pp. 158–64.
