The cell cycle and retinal histogenesis fidget mutant mice.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M V Sazhina.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The eye development has been studied in the 12-day-old, 14-day-old embryos and in neonates of Cm/+ ak/ak genotype. The gene coloboma (Cm) in heterozygous state causes a typical coloboma of the iris and the gene aphakia (ak) blocks the lens development in the homozygotes. It has been shown that in Cm/+ ak/ak mice the eyes go through mainly the same abnormal development as that in +/+ ak/ak animals. In mice of both genotypes the lens morphogenesis blocking at the vesicle stage and the retinal fold in the dorsal half of the eye develops. However, the ventral retinal fold which is characteristic for the +/+ ak/ak mice does not form in the Cm/+ ak/ak animals that is the result of the interaction of Cm and ak genes in the eye morphogenesis. The Cm gene suppressing the growth of the retina ventral half inhibits the formation of its fold in Cm/+ ak/ak embryos. As a result of the gene interaction a certain normalization of the eye development compared to the +/+ ak/ak mice is observed in the Cm/+ ak/ak animals. The obtained data show that the Cm gene expresses in the cell clones of the retina ventral half.
The Miwh expression was studied using a genetical marker, acid beta-galactosidase, in 20 day old chimeric mice Miwh/Miwh Bglb/Bglb C/C in equilibrium +/+ Bgld/Bgld C/Ca and Miwh/Miwh Bglb/Bglb C/C in equilibrium +/+ Bgld/Bgld c/c. Three phenotypically new types of the retinal pigment epithelium (RPE) regions were found in the chimeras, which were absent in the RPE of the parental strains. The presence in the chimeras of the RPE regions consisting of pigmented and normally differentiated cells with a high activity of the enzyme suggests the normalization of differentiation of the Miwh/Miwh RPE cells, due, apparently, to the inducing influence of the normal (+/+ C/C) mesenchyme cells. In addition, the presence of nonpigmented, both hyperplasied and nonhyperplasied, RPE regions (+/+ C/C) suggests an insufficient growth-inhibiting influence and the absence of melanogenesis-stimulating activity of defective Miwh/Miwh ectomesenchyme. The histochemical and cytological analysis of the RPE in the obtained chimeras has, thus, shown that the Miwh gene primarily affects ectomesenchyme, which does not exert melanogenesis-stimulating and growth-inhibiting influence on the RPE ensuring its hyperplasia and the absence of pigmentation.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The effects of paraorbital +/+ and Mi wh/Mi wh mesenchyme (PM) on melanogenesis of the retinal pigment epithelium (RPE) of mouse embryos. The eye anlagen of 10-day-old +/+ and Mi wh/Mi wh mouse embryos were co-cultured in vitro during eight days. All eye anlagen of +/+ genotype without PM cocultured with anlagen of +/+ genotype with PM developed a pigmentation of RPE. However, the eye anlagen of +/+ genotype without PM and the eye anlagen of Mi wh/Mi wh genotype with PM when co-cultured did not develop pigmentation of RPE. These results indicate that mutant allele Mi wh of locus mi changes the properties of PM which in mutant embryos does not exert the normal melanogenesis-promoting effect in relation to RPE.
Explore the source record for details and available documents.
Ultrastructure of cells of the outer root sheath (ORS) of the guard hair follicles from the dorsal part of the body of 12-day old we/we and +/+ mice was studied. Changes observed in the ultrastructure of ORS cells in mutant mice included greater vacuolization of the cytoplasm and damaged structure of mitochondria accompanied by the absence of crisis. Many cells of the ORS outer layer in hair follicles of we/we and +/+ mice showed electron-dense outgrowths oriented axo-proximally which suggests their possible involvement in transportation of the hair, by contraction of these outgrowths, to the skin surface. Possible mechanisms of hair growth in view of these data are discussed.