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.
Isaev DA, Platonov ES, Koniukhov BV. [The distribution of parthenogenetic clones of epidermal melanoblasts in chimeric mice C57BL/6(PG) BALB/c]. Ontogenez. 1997 Jul-Aug;28(4):306-13. Russian. PubMed PMID: 9304094.

The mutant gene wellhaaring (we) confers the waved coat in mice, which is most pronounced in homozygotes at 10 to 21 days of postnatal development. Abnormal hair growth and structure in the we/we mutant mice results from defective cell differentiation in the inner root sheath of a hair follicle. To localize the site of the we gene action, we obtained ten chimeric mice by aggregation of the early C57BL/6-2we/we and BALB/c embryos. The chimera coat was waved, shaggy, or almost normal depending on the percentage of the mutant component. In the we/we +/+ chimeric animals of the first generation (G1) aged 21 days, both mutant and normal hair phenotypes were observed, which was especially discernible in zigzag hair. Note that none of the chimeras exhibited the alternating patterns of transversely oriented stripes or patches of either mutant or normal hair; i.e., they had a mixed parental hair phenotype. We also did not observe the animals with an intermediate phenotype, which suggests a discontinuous hair formation in chimeras according to the "all or nothing" principle. The data obtained indicate that the dermal papilla cells of a hair follicle are the sites for the we gene action. During the embryonic development, dermal cells are strongly mixed, which accounts for the lack of the clear-cut transverse stripes of either mutant or normal hair. The mutant gene we is probably responsible for a disrupted induction signal from the dermal papilla towards ectodermal cells of a hair follicle.
Martynova MIu, Isaev DA, Koniukhov BV. [Effects of the mutant gene wellhaarig in chimeric mice]. Genetika. 2002 Nov;38(11):1511-7. Russian. PubMed PMID: 12500677. (DOI: 10.1023/A:1021151211999)