Gametic Imprinting in Mammals

Science ◽  
1995 ◽  
Vol 270 (5242) ◽  
pp. 1610-1613 ◽  
Author(s):  
D. P. Barlow
Keyword(s):  
Gametic Imprinting

scholarly journals The Mouse Xist Gene: a Model for Studying the Gametic Imprinting Phenomenon

1996 ◽  
Vol 45 (1-2) ◽  
pp. 199-204 ◽  
Author(s):  
M. Zuccotti ◽  
M. Monk
Keyword(s):  
Molecular Mechanisms ◽  
Epigenetic Modification ◽  
Somatic Tissue ◽  
Paternal Allele ◽  
The Status ◽  
Intron Region ◽  
Exon 11 ◽  
Region 10 ◽  
Gametic Imprinting

In mammals, normal embryonic development requires differential genomic imprinting of male and female gametes [1, 2]. Many investigations have been directed towards the understanding of the molecular mechanisms of imprinting and the timing of establishment of the imprint during gametogenesis and its erasure during development.Methylation is the focus of many of these studies as it has been known for some time that this epigenetic modification of the DNA correlates with the status of gene activity. So far, five imprinted genes, expressed from only one of the parental alleles, have been found to be differentially methylated in somatic tissue: mouse Igf2 [3] and Xist [4] and human SNRPN [5, 6] expressed from the paternal allele; mouse Igf2r [7] and H19 [8, 9] expressed from the maternal allele. However, so far, a gametic methylation imprint has been detected for only two of these genes: in an intron region of mouse Igf2r [7], and in the promoter region [10] and the first exon [11] of the Xist (X-inactivation-specific transcript [12, 13] gene.The data accumulated for the Xist gene, during different phases of gametogenesis and development, provides the most comprehensive story about the role of methylation as a primary gametic imprint, and on the timing of its establishment during gametogenesis and erasure during development. Methylation studies have now been performed during oogenesis and spermatogenesis [Norris et al., 1994; 11] and in mature gametes and during early stages of development [10, 11]. In addition, expression of the gene has been described during gametogenesis [14-16] and throughout early development [4-17].

Basics of gametic imprinting

1999 ◽  
Vol 77 (suppl_2) ◽  
pp. 228 ◽  
Author(s):  
A. Ruvinsky
Keyword(s):  
Gametic Imprinting

Mouse oocytes injected with testicular spermatozoa or round spermatids can develop into normal offspring

Development ◽  
1995 ◽  
Vol 121 (8) ◽  
pp. 2397-2405 ◽  
Author(s):  
Y. Kimura ◽  
R. Yanagimachi
Keyword(s):  
Polar Body ◽  
Experimental Conditions ◽  
Male And Female ◽  
Testicular Spermatozoa ◽  
Mouse Oocytes ◽  
Foster Mothers ◽  
Sperm Nuclei ◽  
Second Polar Body ◽  
Normal Offspring ◽  
Gametic Imprinting

Genomic imprinting occurs in both male and female gametes during gametogenesis, but the exact time when imprinting begins and ends is unknown. In the present study we injected nuclei of testicular spermatozoa and round spermatids into mature mouse oocytes to see whether these nuclei are able to participate in syngamy and normal embryonic development. If the injected oocytes develop into normal fertile offspring, imprinting in the male germ cells used must have been completed by the time of injection. Ninety-two percent of mouse oocytes injected with testicular spermatozoa survived and 94% of these were fertilized normally (extrusion of the second polar body and formation of male and female pronuclei). When 44 two-cell embryos so created were transferred to 5 foster mothers, 24 (54.5%) developed into normal offspring. Unlike testicular spermatozoa, round spermatids could not activate the oocytes, and therefore the oocytes had to be activated artificially either before or after spermatid injection. The highest rate (77%) of normal fertilization was obtained when the oocytes were first activated by electric current, then injected individually with a single spermatid nucleus. When 131 two-cell embryos were transferred to 15 foster mothers, 37 (28.2%) reached full term. All but two grew into healthy adults. Thus, it would appear that gametic imprinting in mouse spermatogenic cells is completed before spermiogenesis begins. Under the experimental conditions employed, spermatid nuclei were less efficient than testicular sperm nuclei in producing normal offspring, but perhaps this was due to technical rather than inherent problems.

Gametic imprinting and the manifestation of the fused gene in the house mouse

1990 ◽  
Vol 11 (4) ◽  
pp. 263-269 ◽  
Author(s):  
Anatoly O. Ruvinsky ◽  
Alexander I. Agulnik
Keyword(s):  
House Mouse ◽  
Gametic Imprinting ◽  
Fused Gene

Gametic imprinting effects on rate and composition of pig growth

1994 ◽  
Vol 88 (8) ◽  
pp. 1037-1042 ◽  
Author(s):  
A. G. de Vries ◽  
R. Kerr ◽  
B. Tier ◽  
T. Long ◽  
T. H. E. Meuwissen
Keyword(s):  
Gametic Imprinting

scholarly journals Embryo and Endosperm Development Is Disrupted in the Female Gametophytic capulet Mutants of Arabidopsis

Genetics ◽  
2002 ◽  
Vol 162 (4) ◽  
pp. 1911-1925
Author(s):  
Paul E Grini ◽  
Gerd Jürgens ◽  
Martin Hülskamp
Keyword(s):  
Seed Development ◽  
Transgene Expression ◽  
Female Gametophyte ◽  
Higher Plants ◽  
Embryo Sac ◽  
Endosperm Development ◽  
Wild Type ◽  
Paternal Genome ◽  
Early Stages ◽  
Gametic Imprinting

Abstract The female gametophyte of higher plants gives rise, by double fertilization, to the diploid embryo and triploid endosperm, which develop in concert to produce the mature seed. What roles gametophytic maternal factors play in this process is not clear. The female-gametophytic effects on embryo and endosperm development in the Arabidopsis mea, fis, and fie mutants appear to be due to gametic imprinting that can be suppressed by METHYL TRANSFERASE1 antisense (MET1 a/s) transgene expression or by mutation of the DECREASE IN DNA METHYLATION1 (DDM1) gene. Here we describe two novel gametophytic maternal-effect mutants, capulet1 (cap1) and capulet2 (cap2). In the cap1 mutant, both embryo and endosperm development are arrested at early stages. In the cap2 mutant, endosperm development is blocked at very early stages, whereas embryos can develop to the early heart stage. The cap mutant phenotypes were not rescued by wild-type pollen nor by pollen from tetraploid plants. Furthermore, removal of silencing barriers from the paternal genome by MET1 a/s transgene expression or by the ddm1 mutation also failed to restore seed development in the cap mutants. Neither cap1 nor cap2 displayed autonomous seed development, in contrast to mea, fis, and fie mutants. In addition, cap2 was epistatic to fis1 in both autonomous endosperm and sexual development. Finally, both cap1 and cap2 mutant endosperms, like wild-type endosperms, expressed the paternally inactive endosperm-specific FIS2 promoter GUS fusion transgene only when the transgene was introduced via the embryo sac, indicating that imprinting was not affected. Our results suggest that the CAP genes represent novel maternal functions supplied by the female gametophyte that are required for embryo and endosperm development.

Prenatal fate of parthenogenetic cells in mouse aggregation chimaeras

Development ◽  
1987 ◽  
Vol 101 (1) ◽  
pp. 67-71 ◽  
Author(s):  
A. Nagy ◽  
A. Paldi ◽  
L. Dezso ◽  
L. Varga ◽  
A. Magyar
Keyword(s):  
Early Development ◽  
Tissue Differentiation ◽  
Strong Selection ◽  
Gametic Imprinting ◽  
Key Steps ◽  
Selective Process

Parthenogenetically activated BCF1 and fertilized BALB/c embryos were aggregated to form chimaeras. The fate of the parthenogenetic component was followed in the conceptus during the second half of gestation. The results indicate an early strong selection against parthenogenetic cells in the extra-embryonal part, which is presumably complete by term, and a weaker selective process in the embryo. During early development, parthenogenetic cells have nearly normal developmental potency in the embryo, which allows their balanced contribution in the chimaeras on day 12. Later, this contribution declines significantly resulting in an unbalanced relation to the advantage of the fertilized counterpart. From the results, we suggest that gametic imprinting may play a role not only in the key steps of preimplantation and early postimplantation development, but later in cell and tissue differentiation.

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