Morphofunctional evaluation of the effect of transplantation of allogeneic fibroblasts on healing of burn wounds in albino outbred mice and mutant Hr(hr)/Hr(hr) mice.

Morphofunctional evaluation of the effect of transplantation of allogeneic fibroblasts on skin regeneration after burn injury in albino outbred mice and mutant Hr(hr)/Hr(hr) (nude) mice was carried out using the radioautographic method. The pronounced stimulating effect of allogeneic fibroblasts on healing of burn wound observed in mice of both groups can be attributed to the action of bioactive substances released from destructed allogeneic fibroblasts and stimulating proliferation of stem/progenitor cells in the wound (epithelial cells in skin appendages and dermal cells in microvessel walls) at the early stages of healing.

Morphofunctional evaluation of the effect of collagen-1-based dressing on skin regeneration after burn trauma in mice of two genetic strains.

Morphofunctional evaluation of the effect of biological dressing with collagen-1 on healing of 3A degree burn wound in outbred and mutant Hr(hr)/Hr(hr)(hairless) mice was carried out by the histological method and optic radioautography. A pronounced stimulatory effect of the dressing on skin regeneration in mice was demonstrated. According to radioautography data, early dressing of the burn wounds in Hr(hr)/Hr(hr)mice led to active proliferation of epithelial cells in dermal cyst and vascular endotheliocytes. The possible mechanisms of the stimulatory effect of collagen-based dressing on wound healing are discussed.

[Dermal cysts participate in reparative regeneration of epidermis in Hr(hr)/Hr(hr) mice].

One of the phenotypic effects of mutation in the Hr gene in mice is disintegration of hair follicles and their degeneration into open funnel-shaped structures (utricles) opened on skin surface and cysts located in the depth of the dermis. The aim of the current study consists in analysis of the process of reparative regeneration of skin in homozygotous mice with one of the mutant alleles of the Hr gene-Hr(hr). It is shown that epithelial cells that constitute the inner pavement of cysts take part in the process of epithelization of deep skin wounds. This indicates that the competence of ectodermal cells in relation to inductive signals from injured skin remains in Hrr homozygote mice, in spite of the significant anatomic abnormalities of the hair follicles.

[Effect of 5-azadeoxycytidine and retinoic acid on expression of genomic imprinting in parthenogenetic mouse embryos].

The action of two types of substances has been studied: 5-azadeoxycytidine and retinoic acid, which have a demethylation effect on DNA in the development process of diploid parthenogenetic mouse embryos. The effect of 5-azadeoxycytidine on hybrid mice (CBAxC57BL/6)F1 in vitro for 6 h, in the presence of single cell parthenogenetic embryos during the S-phase of the cell cycle has been studied. After developing to the blastocyst stage in vitro, parthenogenetic embryos were transplanted into the uterus of false pregnant females. It has been determined that a concentration of 0.1 microM 5-azadeoxycytidine activates embryonic development in the preimplantation period until the blastocyst stage (69% in experiment; 61% in the control) and during postimplantation, it increases the number of available space in the uterus for implantation (76% in experiment; 63% in the control). The effect of retinoic acid on parthenogenetic embryos from inbred C57BL/6 or CBA mice lines was studied by adding it to single cell embryos in a medium in vitro for 96 h. Treating parthenogenetic embryos C57BL/6 with retinoic acid concentrations 0.1 microM or 0.5 microM significantly increased the number of spaces for embryo implantation, 76% and 78% respectively, as against 57% for untreated embryos. Addition of similar doses of retinoic acid to the nutrient medium containing CBA parthenogenetic mouse embryos does not improve implantation (as with embryos C57BL/6), and a concentration of 2.0 microM is toxic to the embryos. During the period of postimplantation, parthenogenetic embryos of mouse lines C57BL/6 treated with retinoic acid just as the controls, did not develop to the somite stage. Mouse lines CBA had 45% of their embryos which were used as controls, developing to the advanced somite stages. However, the number of embryos treated with retinoic acid does not increase. Thus the treatment of two parthenogenetic embryos from inbred mice lines and their hybrids with compounds which demethylate DNA (5-azadeoxycytidine and retinoic acid) creates an opportunity for partial modulation of genomic imprinting and an increase in the survival rate of such embryos.

[Expression of imprinted Igf2 and Peg1/Mest genes in postimplantation parthenogenetic mouse embryos treated with transforming growth factor alpha in vitro].

The effect of transforming growth factor alpha (TGFt) on the expression of imprinted Igf2 and Peg1/Mest genes was studied in diploid parthenogenetic embryos (PEs) of (CBA x C57BL/6)F1 mice during the postimplantation period of embryogenesis. The PEs were treated with TGFalpha in vitro at the morula stage and, after they developed to the blastocyst stage, were implanted into the uterus of false-pregnant females. On the tenth day of pregnancy, the PEs were explanted for subsequent in vitro culturing for 24 or 48 h. The expression of the imprinted Igf2 and Peg1/Mest genes was studied by means of whole mount in situ hybridization using digoxigenin-labeled antisense RNAs. The expression of the imprinted Igf2 and Peg1/Mest genes was studied in embryos on the tenth day of in utero development before culturing and after 24 and 48 h of culturing in vitro. The expression of Igf2 before culturing was detected only in the brain of 60% of PEs on the tents day of pregnancy (the 21-to 25-somite stages); while the Peg1/Mest expression was not detected at all. In control (not treated with TGFalpha) PEs, neither gene was expressed at the same 21- to 25-somite stages. After 24 h of culturing, the Igf2 expression was detected in the brain of 71% of PEs at the 30- to 35-somite stages, while the Peg1/Mest expression was not detected. In control (untreated) PEs, neither imprinted gene was expressed at the 30- to 35-somite stage. After 48 h of culturing, Igf2 was expressed in the regions of the brain, developing jaws, heart, liver, and somites of all TGFalpha-treated PEs at the 40- to 45-somite stages; and Peg1/Mest was expressed in the brain, heart, and liver of these embryos. In control (untreated) PEs, neither Igf2 nor Peg1/Mest was expressed at these stages The expression patterns of the imprinted Igf2 and Peg1/Mest genes in PEs at the most advanced developmental stages (40-45 somites) and in normal (fertilized) embryos at the same stages were similar; however, their expression rate in PEs was substantially lower than in normal embryos. These data indicate that exogenous TGFalpha can reactivate the expression of the two imprinted genes, modulating the effects of genomic imprinting in such a way that the PE development is improved and substantially prolonged.

[Genomic imprinting in the epigenetics of mammals].

Genomic imprinting is one of the most remarkable and important epigenetic phenomena. A biological ban on parthenogenetic and androgenetic development of mammals is an obvious consequence of genomic imprinting. Genomic imprinting defects may cause malformations, clinical syndromes, and tumor growth in humans and to the large offspring syndrome and an increased mortality after in vitro manipulations with early embryos in mammals. Differential expression of parental alleles during ontogeny implies a mechanism of reversible, selective marking of gene alleles. These relatively stable epigenetic modifications, which do not affect the primary nucleotide sequence of DNA, may be transmitted in somatic cell lines and reproduced in the germ line. The genomic imprinting mechanism may be involved in other epigenetic processes, such as epigenetic inheritance, nonrandom allele segregation, meiotic drive, etc. Artificial modulation of genomic imprinting effects with the use of growth factors and demethylating agents permits partial "normocoping" during the development of parthenogenetic mouse embryos. Targeted changes in the transcriptional activity of imprinted genes provide prerequisites for epigenetic correction of syndromes and diseases caused by genomic imprinting defects.

TGFalpha reactivates imprinted Igf2 in the parthenogenetic mice embryos and placenta.

Imprinted genes play important roles in the mammalian development. In the parthenogenetic embryos (PE) there is only expression of maternally expressed genes. Therefore, PEs are appropriate experimental models to study genomic imprinting controlling mechanisms. The maternally expressed H19 and paternally expressed Igf2 are reciprocally imprinted genes in normal embryos. Here we studied effect of transforming growth factor alpha (TGFalpha) treatment in vitro (10 ng/ml at the morula stage) on the expression of Igf2/H19 locus in mice PE (9.5-days of gestation, 25 somites) and their placentas (PP). Using RT-PCR we showed that TGFalpha reactivated maternally imprinted Igf2 gene in parthenogenetic embryos and placentas. In spite of similar Tgfalpha expression in the pre-implantation stages, its expression in the 9.5-day parthenogenetic embryos is significantly less than in normal embryos (NE). In our experiments it was shown that reactivation of Igf2 gene occurred independently of H19 gene. In vitro TGFalpha treatment of mouse PE reactivated paternally expressed Igf2 gene in the PE and PP. In the PE and PP both Igf2 and H19 were expressed. It seems that TGFalpha can play an important role as modulator of the Igf2/H19 locus.

[Genomic imprinting and problem of parthenogenesis in mammals].

Genomic imprinting belongs by its nature to problems of epigenetics, which studies hereditary changes in gene expression not related to defective sequences of DNA nucleotides. Epigenetic mechanisms of control, including genomic imprinting, are involved in many processes of normal and pathological development of humans and animals. Disturbances of genomic imprinting may lead to various consequences, such as formation of developmental anomalies and syndromes in humans, appearance of the large offspring syndrome and increased mortality upon cloning of mammals, and death of parthenogenetic embryos soon after implantation and beginning of organogenesis. The death of diploid parthenogenetic or androgenetic mammalian embryos is determined by the absence of expression of the genes of imprinted loci of the maternal or paternal genome, which leads to significant defects in development of tissues and organs. A review is provided of the studies aimed at search of possible normalization of misbalanced gene activity and modulation of genomic imprinting effects during parthenogenetic development in mammals.

[Effects of growth factors FGF4, TGFalpha, and TGFbeta1 on the development of parthenogenetic embryos of C57BL/6 mice].

We studied the effects of three growth factors, fibroblast growth factor (FGF4), transforming growth factor alpha (TGFalpha), and transforming growth factor beta1 (TGFbeta1), on development of diploid parthenogenetic embryos of C57BL/6 mice, which are not capable of developing to somatic stages. Parthenogenetic embryos were treated with growth factors at optimal doses in vitro at the morula--blastocyst stages and transplanted in the uterus of pseudopregnant females. FGF4 and TGFalpha improved the development of parthenogenetic embryos at the preimplantation stages and the number of blastocysts increased under the influence of TGFalpha. All three growth factors improved the implantation of embryos in the uterus. When FGF4 or TGFbeta1 were added to the nutrient medium, 2.4 or 1.6%, respectively, of parthenogenetic embryos reached the somatic stages in utero. No somitic embryos were observed in the control. The treatment of parthenogenetic embryos with two growth factors, FGF4 and TGFbeta1, simultaneously increased the amount of somatic embryos to 7.5%, while combination of three growth factors in creased the amount of such embryos to 16.7%. In the latter case, some parthenogenetic embryos reached the stage of 25-27 pairs of somites and were 2.0-2.5 mm long. The data we obtained suggest that, when combined, the growth factors FGF4, TGFalpha, and RGFbeta1 possessed a synergistic effect leading to a significant improvement of the development of parthenogenetic C57BL/6 embryos.

[Leukemia inhibitory factor (LIF) improves and prolongs the development of parthenogenetic mouse embryos]. / Faktor ingibirovaniia leikemii (LIF) uluchshaet i prolongiruet razvitie partenogeneticheskikh zarodyshei myshei.

We studied the effect of the growth factor LIF on the development of parthenogenetic mouse embryos (CBA x C57BL/6)F1. LIF was added to the culture medium at 10, 50, 100, and 250 ng/ml at the morula stage and parthenogenetic embryos were cultivated in vitro until the late blastocysts stage and then transplanted in the uterus of pseudopregnant females, which were then sacrificed on day 12 of pregnancy. All the LIF doses used improved the development of parthenogenetic mouse embryos at the preimplantation stages and increased the amount of blastocysts by 16%, on average, as compared to the control. LIF at 50 and 100 ng/ml increased approximately twice the number of embryos that reached the somatic stages. Some of them reached the stage of 32-45 somites and had fore and hind limb buds. No such embryos were found in the control. Well formed placenta was observed in 6% of the embryos treated with LIF and the most pronounced effect was recorded at 100 ng/ml. The data we obtained suggest that exogenous LIF can improve pre- and postimplantation development of parthenogenetic mouse embryos due, possibly, to increased survival rate of embryonic stem cells derived from the inner cell mass of blastocysts. LIF improves not only the development of the parthenogenetic embryo per se, but also the formation of its extraembryonic envelopes, which leads to the development of a larger placenta in LIF-treated parthenogenetic embryos, as compared to the control.

[Effects of growth factors FGF2 and IGF2 on the development of parthenogenetic mouse embryos in utero and in vitro]. / Deistvie rostovykh factorov FGF2 i IGF2 na razvitie partenogeneticheskikh c'mbrionov myshei in utero i in vitro.

We studied the effects of fibroblast growth factor 2 (FGF2) and insulin-like growth factor 2 (IGF2) on the development of parthenogenetic mouse embryos (CBA x C57BK/6)F1. The parthenogenetic embryos were treated in vitro during the preimplantation period and, at the blastocyst stage, transplanted into the uterus of pseudopregnant females. The addition of FGF2 at an optimal dose (2.5 ng/ml) to the culture medium increased twofold the number of embryos developed in utero to the somite stages as compared to the control: 18 and 43%, respectively. The parthenogenetic embryos (18-21 somites), treated and nontreated with FGF2 during the preimplantation period, were explanted for further development in vitro and treated with IGF2 at 2.5 micrograms/ml. As a result, many more parthenogenetic embryos (> 87%) of both groups developed in vitro to the stage of 30 or more somites as compared to the control (59%). The treatment of the parthenogenetic embryos with FGF2 alone at the preimplantation stages did not improve their development in vitro at the postimplantation stages. The results we obtained suggest that the treatment of parthenogenetic embryos in vitro with FGF2 during the preimplantation period increased twofold the number of somite embryos in utero, while their subsequent treatment in vitro with IGF2 leads to a significant prolongation of their development, as compared to the control.

Effects of fibroblast growth factor 2 and insulin-like growth factor II on the development of parthenogenetic mouse embryos in vitro.

Most parthenogenetic embryos (PEs) in mammals die shortly after implantation, and this failure to develop is associated with genomic imprinting. We have examined the influence of human recombinant basic fibroblast growth factor 2 (FGF-2) and human recombinant insulin-like growth factor II (ICF-II) on the development of (CBA x C57BL/6)F1 parthenogenetic mouse embryos. Embryos were treated in vitro at the morula stage with different doses of FGF-2 and, after their development to blastocysts, transferred to pseudopregnant recipients. The optimal doses of FGF-2 did not affect the number of forming and implanting blastocysts, but increased, from 20 to 42%, the number of embryos developing to somite stages. PEs (18-21 somites) treated with an optimal dose of FGF-2 were explanted for further development in culture by treatment with the second growth factor, IGF-II. Eighty-three percent of those embryos cultured with IGF-II (2.5 microg/ml) developed to 35 or more somites, as compared with 36% of embryos cultured without any growth factors (P < 0.01). Also, a significantly higher proportion of PEs developed to 40-50 somites in this case. These results show that the in vitro treatment of PEs with FGF-2 at the morula stage increases the number of somite embryos, and the second treatment of somite PEs with IGF-II in culture medium prolongs their development significantly.

[Genomic imprinting in mammals]. / Genomnyi imprinting u mlekopitaiushchikh.

A review of the data on the mechanisms and effects of genomic imprinting, an epigenetic phenomenon regulating the development in placentate mammals, is presented. In contrast to the majority of gene loci with biallelic expression, the expression of imprinted loci is monoallelic. In humans and mice, more than 300 imprinted loci have been identified, in which maternal or paternal alleles may either be expressed or be found in a repressed state during ontogeny. Imprinting is established during gametogenesis, and the repression of an allele of the imprinted locus is determined by methylation of the key regulatory element of this allele. Both the maternal and paternal chromosome sets are required for normal development in mammals. This is why parthenogenesis and androgenesis in these animals are impossible in nature. As a result of differential gene expression of many imprinted loci, the balance of gene activity is established, which is necessary for normal proliferation and differentiation of various cell clones in embryogenesis. Many human developmental abnormalities and syndromes are determined by defective genomic imprinting. In particular, the loss of imprints, which is followed by the occurrence of biallelic expression of some imprinted loci, may cause malignant tumors.

[Transforming growth factor alpha (TGFalpha) modulates the effect of genomic imprinting and prolongs the development of parthenogenetic murine embryos]. / Transformiruiushchii rostovoi faktor alpha (TGFalpha) moduliruet éffekty genomnogo imprintinga i prolongiruet razvitie partenogeneticheskikh émbrionov myshei.

The effect of transforming growth factor alpha (TGF alpha) on the development of diploid parthenogenetic mouse embryos (CBA x C57BL/6)F1 was studied. The embryos were in vitro treated with the TGF alpha at the stage of morula. Upon reaching the blastocyst stage, each embryo was implanted into uterus of a pseudopregnant female. At a dose of 5 ng/ml, the TGF alpha was found to improve development of parthenogenetic embryos before implantation, increase significantly the number of developing blastocysts, and promote embryo implantation into uterus. After treatment with TGF alpha at a dose of 10 ng/ml, 4% of parthenogenetic embryos reached the stage of 30-45 somites and had forelimb and hindlimb buds; the embryo size from vertex to sacrum was 2.0 to 3.8 mm. A well-developed placenta was observed in 6% of TGF alpha-treated parthenogenetic embryos that reached the somite stages. In the parthenogenetic embryos with the most prominent development (42-45 somites) treated with 10 ng/ml of TGF alpha, the placental diameter was 4.0 to 4.2 mm on day 12 of gestation, which is close to the placental size of the normal (fertilized) 11-day-old mouse embryos. Our results suggest that endogenous TGF alpha can modulate the effects of genomic imprinting significantly improving formation of trophoblast derivatives and promoting longer postimplantation development of parthenogenetic embryos.

[An analysis of parthogenetic cell clones in chimeric C57BL/6(PG)<-->BALB/c mice]. / Analiz partenogeneticheskikh kletochnykh klonov u khimernykh myshei C57BL/6(PG)<-->BALB/c.

We studied the distribution of parthenogenetic cell clones in the retinal pigment epithelium and choroid of eyes on serial sections and in the brain, kidneys, and liver by electrophoretic analysis of glucose phosphate isomerase isozymes in 12 mouse chimeras C57BL/6(PG)<-->BALB/c obtained earlier. Asymmetry was noted in the distribution of the parthenogenetic cell clones in the eye structure, just as the earlier established asymmetry in the distribution of the parthenogenetic clones of epidermal melanoblasts. A high correlation was shown between the ratio of parthenogenetic to normal cells in the retinal pigment epithelium of the right or left eyes and epidermal melanoblasts in the hair cover of the corresponding body half of the chimera. These data suggest that there is a certain relationship between the processes leading to the characteristic distribution of the ectodermal parthenogenetic clones in the retinal pigment epithelium of the right and left eyes and epidermal melanoblasts in parthenogenetic chimeras. Electrophoretic analysis did not show parthenogenetic components in the liver or kidneys of any chimera, and the parthenogenetic component was found in the brain of only two chimeras, in which a high percentage of parthenogenetic cells of ectodermal origin was noted. In these cases, asymmetry was noted in the right and left cerebral hemispheres, just as in the retinal pigment epithelium of the right and left eyes. The data obtained suggest that, during the development of the chimeras, parthenogenetic C57BL/6 cells were actively eliminated from the tissues of endodermal and mesodermal origin. In adult chimeras C57BL/6(PG)<-->BALB/c, parthenogenetic cell clones of ectodermal origin are mostly preserved.

[The effect of fibroblast growth factors (FGF-2, FGF-4) on the development of parthenogenetic mouse embryos]. / Vliianie faktorov rosta fibroblastov (FRF-2, FRF-4) na razvitie partenogeneticheskikh émbrionov myshchei.

We studied the effects of two growth factors, FGF-2 and FGF-4, on development of diploid parthenogenetic mouse embryos (CBA x C57BL/6)F1. Parthenogenetic embryos were treated with FGF-2 or FGF-4 in vitro at the morula stage and, after they reached the blastocyst stage, transplanted into the uteri of pseudopregnant females. FGF-2 and FGF-4 did not affect the number of blastocysts formed in vitro or implantation into the uterus. However, FGF-2 and FGF-4 at optimal doses decreased the mortality rate of parthenogenetic embryos at the early postimplantation stages and increased twofold the number of embryos that developed in utero to the somite stages: 42 and 36%, respectively, versus 20% in the control. The results obtained suggest that the treatment of parthenogenetic mouse embryos with FGF-2 or FGF-4 modulate the effects of genomic imprinting and prolong the development of parthenogenetic embryos at the postimplantation stages.

[The distribution of parthenogenetic clones of epidermal melanoblasts in chimeric mice C57BL/6(PG) <--> BALB/c]. / Raspredelenie partenogeneticheskikh klonov épidermal'nykh melanoblastov u khimernykh myshei C57BL/6(PG) <--> BALB/c.

The death of diploid parthenogenetic mammalian embryos, specifically mouse embryos, is related to the effects of genomic imprinting. But in mouse chimeras, many parthenogenetic cell clones retain their viability for long periods of development. We obtained 12 chimeric mice by aggregating diploid parthenogenetic C57BL/6 (C/C) embryos with normal BALB/c (c/c) embryos at the 8-cell stage. Distribution of parthenogenetic clones of the melanoblasts in the hair follicles of chimeric mice was estimated by the presence of pigmented regions of the hair cover. The proportion of pigmented regions of the hair cover did not exceed 35% in any of 12 parthenogenetic chimeras C57BL/6(PG) <--> BALB/c. In most chimeras, pigmented regions were present in the anterior and posterior parts of the body. At the same time, the middle part of the body was, as a rule, not pigmented, possible due to the death of parthenogenetic melanoblasts in this area. In many chimeras, bilateral distribution of pigmented regions was disturbed, possibly due to accidental death of individual parthenogenetic clones of the melanoblasts. The absence of pigmentation of the ventral body side and distal parts of the limbs in most obtained chimeras appears to be due to decreased proliferative activity of the parthenogenetic melanoblasts, as compared with the normal situation.

[Ultroser-G and 5-azacytidine prolong the development of parthenogenetic mouse embryos]. / Ul'troser-G i 5-azatsitidin prolongiruiut razvitie partenogeneticheskikh zarodyshei myshei.

We studied the effects of Ultroser-G, a substitute of embryonal serum, and 5-azacytidine, a DNA-demethylating compound, on development of diploid parthenogenetic embryos of the mouse inbred strain CBA and hybrids (CBA x C57BL/6)F1. Addition of Ultroser-G to the nutrient medium for in vitro cultivation of the embryos to a final concentration of 0.5% leads after their transplantation into the uterus of pseudopregnant females to development of parthenogenetic postimplantation embryos to a stage of 30-33 somites with the buds of fore- and hindlimbs. Additional introduction of 5-azacytidine at 0.24 mg/kg to the females on day 8 of gestation prolonged development of some parthenogenetic embryos treated with Ultroser-G during the preimplantation period to the stage of 45 somites. The control embryos developed to the stage of 25 somites. The mechanism of genomic imprinting and influence of the embryonal serum components and demethylating compounds on viability of the parthenogenetic embryos are discussed.

Prolonged development of normal and parthenogenetic postimplantation mouse embryos in vitro.

Parthenogenetic mammalian embryos show reduced placental development and do not develop beyond the 25-somite stage. But non-parthenogenetic embryos in culture, without a functional placenta, can develop to 40 somites or more. We have therefore examined the possibility that parthenogenetic embryos might also show prolonged development in culture. After parthenogenetic activation and diploidization, 23% of CBA and 56-58% of hybrid (CBAxC57BL/6) F1 mouse eggs developed in culture to blastocysts. When transferred to pseudopregnant recipients: 60% of the CBA blastocysts implanted and 26% of these developed to somite stage embryos; 71-72% of the hybrid blastocysts implanted and 11-17% of these developed to somite stage embryos. Improved development of postimplantation embryos explanted into culture at about the 15-20 somite stage was obtained by opening the visceral yolk sac (without exteriorizing the embryo). All the normal (non-parthenogenetic) embryos cultured in this way developed to more than 35 somites and many reached 45-55 somites. Under the same conditions, 11/17 diploid parthenogenetic CBA embryos developed in culture to more than 35 somites and 5 of these reached 45 somites; and 9/28 diploid parthenogenetic (CBAxC57BL/6) F1 embryos developed to 35 somites or more and 5 of these reached 45 somites. The size and protein content of the parthenogenetic embryos after culture was less than that of the normal embryos of equivalent stages. These results raise new possibilities for the analysis of parthenogenesis and genomic imprinting, including studies of the effects of adding to the culture medium specific growth factors and demethylating agents.

[The development of diploid parthenogenetic mouse embryos of the inbred C57BL and CBA strains]. / Izuchenie razvitiia diploidnykh partenogeneticheskikh zarodyshei myshei inbrednykh linii C57BL i CBA.

We studied preimplantation development in vitro and postimplantation development in vivo of diploid parthenogenetic mouse embryos of C57BL/6 and CBA strains, as well as of (CBA x C57BL/6)F1 hybrids. Development to blastocyst stage of diploid eggs obtained from C57BL/6, CBA, and hybrid mice was observed in 90, 15, and 73% cases, respectively. After implantation, C57BL/6 embryos did not develop to somite stages, while CBA and hybrid embryos reached various stages of somite formation in 45 and 30% cases, respectively. Cultivation of embryos beginning from one-cell stage in the medium containing 2% newborn calf serum increased the yield of blastocysts from 15 to 59% in CBA embryos and from 73 to 90% in hybrids; However, such effect was not observed with C57BL/6 embryos. The latest stages of development observed in CBA and hybrid diploid parthenogenetic embryos were 33-35 somites and 25-30 somites, respectively. Imprinting patterns in chromosomes of CBA and C57BL/6 gametes are discussed.