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Glossary of scientific and technical terms in bioengineering and biological engineering
Published in Megh R. Goyal, Scientific and Technical Terms in Bioengineering and Biological Engineering, 2018
X-inactivation is the repression of one of the two X-chromosomes in the somatic cells of females as a method of dosage compensation; at an early embryonic stage in the normal female, one of the two X-chromosomes undergoes inactivation, apparently at random, from this point on all descendent cells will have the same X-chromosome inactivated as the cell from which they arose, thus a female is a mosaic composed of two types of cells, one which expresses only the paternal X-chromosome, and another which expresses only the maternal X-chromosome.
How the quest to improve sheep reproduction provided insight into oocyte control of follicular development
Published in Journal of the Royal Society of New Zealand, 2018
Unexpectedly, ewes homozygous for the Inverdale mutation were shown to be infertile, typically with small ‘streak’-like ovaries (Davis et al. 1992). This unusual phenotype, with heterozygous ewes having increased ovulation rate and homozygous carriers being infertile, requires a structured approach in commercial use of the gene. It also provided the ability to generate known wild-type, heterozygous and homozygous carriers of the mutation long before the causative mutation was identified (Davis et al. 1992). Physiological studies with these ewes provided clues about potential candidate genes that might underlie the phenotype. For example, histological examination (Braw-Tal et al. 1993; Smith et al. 1997) of the ovaries during both fetal and adult life demonstrated that the mutation did not affect normal formation of ovarian follicles, or the ability to initiate follicular growth (i.e. normal type 2 or primary follicles were observed). However, normal type 3 follicles were never observed and abnormal follicles, with enlarged oocytes and a failure of normal proliferation of granulosa cells, were also noted. This strongly suggested that the protein produced by the mutated gene in the Inverdale animals first became essential in follicular development at the type 2 stage of development. In addition, the fact that ewes heterozygous for the Inverdale mutation did not show any of the abnormal follicles observed in homozygous ewes (Juengel et al. 2000) was consistent with the factor being produced by the oocyte and not granulosa cells. This is because, while X-inactivation occurs in the granulosa cells during the stages of follicular development affected in the homozygous Inverdale ewes, the oocytes express both maternal and paternal copies of the X-chromosome (Dementyeva et al. 2009). Granulosa cells in individual follicles can be derived from a few progenitor cells, and thus some follicles have the same X-chromosome inactivated in all their granulosa cells (Telfer et al. 1988; Van Deerlin et al. 1997). If the gene was expressed exclusively in the granulosa cells, it would be expected that some follicles would only express the inactive protein. Thus, abnormal follicles would sometimes be expected in heterozygous carriers of the mutation if the functionally active protein was expressed only in the granulosa cells. As this was not observed, an oocyte expressed factor was postulated.