This is a review of the data of clonal analysis of developing tissues in parthenogenetic and androgenetic chimeric mice. The time and causes of death of the parthenogenetic and androgenetic cell clones in chimeras are considered. The data obtained suggest that the development of cell clones, derivatives of the mesoderm and endoderm, is determined by the expression of alleles of the imprinted loci of paternal chromosomes, while the formation of cell clones, derivatives of the ectoderm, depends on the expression of other imprinted loci of maternal chromosomes. The death of androgenetic and parthenogenetic (gynogenetic) mammalian embryos is due to the lack of the expression of certain imprinted loci of the maternal and paternal genome, respectively.
Koniukhov BV, Isaev DA. [Use of chimeric mice for studying the effects of genomic imprinting]. Ontogenez. 2000 Sep-Oct;31(5):360-7. Review. Russian. PubMed PMID: 11036671. (DOI: 10.1007/BF02758910)

Clonal analysis of parthenogenetic chimeric mouse embryos C57B1/6(PG)<-->BALB/c has shown that parthenogenetic cell clones C57BL/6 are present in the brain, liver, and kidneys of 14- and 18-day-old embryos. The content of the parthenogenetic component (PG) in these organs on day 18 was lower than on day 14, and, in some 18-day-old embryos, parthenogenetic cell clones were absent from the liver and/or kidneys. These data suggest that, during the embryogenesis of parthenogenetic chimeras, parthenogenetic cell clones of mostly endodermal and mesodermal origins were actively eliminated. Therefore, in such parthenogenetic adult chimeras, parthenogenetic clones of mostly ectodermal origins were preserved. In parthenogenetic chimeras CBA(PG)<-->BALB/c, parthenogenetic cell clones were actively eliminated at early embryonic stages, and, as a result, they were absent at the post-implantation stages. Hence, during development of parthenogenetic cell clones, the effects of genomic imprinting are expressed unequally in C57BL/6 and CBA mice.
Isaev DA, Martynova MI, Platonov EC, Koniukhov BV. [Different influences of genomic imprinting on the development of parthenogenetic cell clones in C57BL/6 and CBA mice]. Ontogenez. 2001 Sep-Oct;32(5):353-9. Russian. PubMed PMID: 11605408. (DOI: 10.1023/A:1012304416799)

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.
Platonov ES, Isaev DA. [Genomic imprinting in the epigenetics of mammals]. Genetika. 2006 Sep;42(9):1235-49. Review. Russian. PubMed PMID: 17100091. (DOI: 10.1134/S1022795406090092)