@article{markert_amet_goldberg_1998, title={Human testis-specific lactate dehydrogenase-C promoter drives overexpression of mouse lactate dehydrogenase-1 cDNA in testes of transgenic mice}, volume={282}, ISSN={["0022-104X"]}, DOI={10.1002/(SICI)1097-010X(199809/10)282:1/2<171::AID-JEZ19>3.3.CO;2-5}, abstractNote={The three isozymes of lactate dehydrogenase, each encoded by a separate gene, are developmentally regulated and differentially expressed in tissue-specific patterns. The lactate dehydrogenase-C (LDHC, mouse Ldh3) gene is temporally expressed exclusively in the germ line during spermatogenesis, whereas lactate dehydrogenase-A (LDHA, mouse Ldh1) and B (LDHB, mouse Ldh2) genes are active in somatic tissues. To determine, therefore, whether overexpression of Ldh1 would perturb spermatogenesis, we constructed a transgene in which a sequence from the promoter region of human LDHC was coupled with mouse Ldh1 cDNA. Among nine (three males, six females) founder lines that were identified as being transgenic for the construct, one male transmitted the gene through its germ line. Homo- and heterotetramers containing the LDH-A subunit were detected in homogenates of testes from transgenic animals. We conclude that the human LDHC promoter contains the necessary regulatory sequence(s) for specific expression of mouse Ldh1 as a transgene during spermatogenesis. The fertility of the founder animal was not impaired. J. Exp. Zool. 282:171–178, 1998. © 1998 Wiley-Liss, Inc.}, number={1-2}, journal={JOURNAL OF EXPERIMENTAL ZOOLOGY}, author={Markert, CL and Amet, TM and Goldberg, E}, year={1998}, month={Oct}, pages={171–178} }
 @article{markert_1989, title={DO INDUCTIVE DEVELOPMENTAL INTERACTIONS OR IMMUNE-REACTIONS DECIDE THE SUCCESS OR FAILURE OF INTERSPECIFIC GESTATIONS}, volume={20}, ISSN={["8755-8920"]}, DOI={10.1111/j.1600-0897.1989.tb00633.x}, abstractNote={.The mammalian embryo is nearly always genetically different from the maternal organism and therefore has th.e properties of an allograft. Yet, the embryo seldom, If .ever, suffers immune rejection. The embryo synthesizes molecules that may be recognized as antigenic by the maternal organism; if the embryo were not protected in the uterus, it would be rejected.P' How does the embryo escape immune rejection by the maternal organism? Clearly, the placenta constitutes an effective barrier even in ectopic pregnancies. How it ~ulfills this role is ~he subject of extensive investigation III many laboratories, but as yet, the protective mechanisms are not clear. The nature of embryo-maternal interactions is sharply presented by interspecific gestations after embryo transplantation to a foreign uterus." Investigators are now transplanting embryos between species for a variety of reasons, including the use of the procedure for the re.scue of endangered species. Unfortunately, these foreign embryos are usually rejected, sometimes very quickly, as in the case of embryos transplanted}, number={1}, journal={AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY}, author={MARKERT, CL}, year={1989}, month={May}, pages={27–28} }
 @article{markert_1988, title={IMPRINTING OF GENOME PRECLUDES PARTHENOGENESIS, BUT UNIPARENTAL EMBRYOS CAN BE RESCUED TO REPRODUCE}, volume={541}, ISSN={["0077-8923"]}, DOI={10.1111/j.1749-6632.1988.tb22300.x}, abstractNote={One legitimate concern in the practice of human in vitro fertilization is that human eggs may be accidentally activated to develop parthenogenetically without any genetic contribution from the sperm. Mammalian eggs are rather easily activated to begin development by a variety of artificial stimulae such as treatment with dilute alcohol, electric shock, cold and heat, incubation in media deprived of certain ions, and so forth.'-3 Mouse eggs obtained from several different inbred strains will sometimes begin to develop parthenogenetically once placed in culture. The provoking stimuli have not yet been identified. A large number of eggs of the mouse strain LT/SV spontaneously begin to develop while still in the o v i d ~ c t . ~ Parthenogenesis can lead either to haploid or to diploid embryos. But in no case have any of these parthenogenetic embryos ever developed to term. In mice, the most extensive development recorded is to the twenty-five somite Most mouse parthenotes die before reaching 10 days of gestation, about halfway through the total gestation period for mice. Parthenogenesis, or more precisely in some species gynogenesis, occurs in all vertebrate classes except for mammals. Even in birds, there are well-documented examples of parthenogenetic development in turkeys7** and in chickens.' Among reptiles, numerous species of lizards are composed only of females." Many of these live in the southwestern part of the United States. Among amphibians and fish, there are also numerous examples of development without any genetic contribution by sperm. The failure of mammals to ever develop parthenogenetically to term, therefore, presents a perplexing problem, although this failure should be reassuring to those involved with human IVF. Nevertheless, it is important to be able to identify in vitro those human eggs that may start to develop parthenogenetically. The attempt to produce the equivalent of mammalian parthenogenesis by microsurgical removal of the male pronucleus" from fertilized eggs coupled with nuclear transplantation techniques has led to a remarkable new insight into the developmental capacity of male and female genomes in the zygote.'*-'' The evidence is now decisive; chromosomes from the male and female parents are imprinted differently during the course of gametogenesis so that at fertilization, the male and female genomes do not function equivalently, even though they may be genetically identical in terms of}, journal={ANNALS OF THE NEW YORK ACADEMY OF SCIENCES}, author={MARKERT, CL}, year={1988}, month={Oct}, pages={633–638} }