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Cloning Tags > Tag based links for Zygote

The following links have been tagged zygote by users just like you, because these resources are off-site we cannot guarantee the accuracy or quality of any third-party information.

  1. The enigma of ATCE1, an acrosome-assoc iated transcription factor.: Dev Biol, Vol. 298, No. 1. (1 October 2006), pp. 201-211.Atce1 belongs to the CREB3/LZIP subtype of the ATF/CREB transcription factor gene family. Its transcription has previously been shown to be testis-specifi c and within the testis to be restricted to haploid spermatids. In this study, we characterized the protein's distribution in the testis and found that it accumulates in late round and in elongating spermatids, corresponding to developmental stages considered transcriptiona lly silent. ATCE1 accumulation is acrosome-speci fic and persists up to mature epididymal cells, at which stage the protein remained associated with the inner acrosome membrane even after acrosomal reaction. No nuclear localization was evident at any spermatogenic stage. Expression of full-length ATCE1 in various cell lines revealed ER and Golgi localization whereas truncation of the C-terminus allowed entrance into the nucleus. Potent transcriptiona l activation activity, from kB-containing regulatory elements (but not from CRE elements as one might expect), was observed using the C-terminally truncated nuclear form of ATCE1. These results raise the question of why would a transcription factor be specifically anchored to the acrosome inner membrane? An intriguing speculation that ATCE1 might be paternally delivered to the newly formed zygote is discussed.S Gil, D Yosef, N Golan, J Don

    Source: Dev Biol, Vol. 298, No. 1. (1 October 2006), pp. 201-211.

  2. A genetic mosaic screen of essential zygotic genes in Caenorhabditis elegans.: Genetics, Vol. 128 (1991), pp. 281-292.We have devised a simple genetic mosaic screen, which circumvents the difficulties posed by phenotypic analysis of early lethal mutants, to analyze essential zygotic genes in Caenorhabditis elegans. The screen attempts to distinguish genes involved in cell type and/or lineage specific processes such as determination, differentiatio n or morphogenesis from genes involved in general processes such as intermediary metabolism by using the pattern of gene function to classify genes: genes required in one or a subset of early blastomeres may have specific functions, whereas genes required in all early blastomeres may have general functions. We found that 12 of 17 genes examined function in specific early blastomeres, suggesting that many zygotic genes contribute to specific early processes. We discuss the advantages and limitations of this screen, which is applicable to other regions of the C. elegans genome.EA Bucher, IS Greenwald

    Source: Genetics, Vol. 128 (1991), pp. 281-292.

  3. The mog-1 gene is required for the switch from spermatogenesi s to oogenesis in Caenorhabditis elegans.: Genetics, Vol. 133 (1993), pp. 919-931.Caenor habditis elegans hermaphrodites make first sperm, then oocytes. By contrast, animals homozygous for any of six loss-of-functi on mutations in the gene mog-1 (for masculinizatio n of the germ line) make sperm continuously and do not switch into oogenesis. Therefore, in mog-1 mutants, germ cells that normally would become oocytes are transformed into sperm. By contrast, somatic sexual fates are normal, suggesting that mog-1 plays a germ line-specific role in sex determination. Analyses of double mutants suggest that mog-1 negatively regulates the fem genes and/or fog-1: mog-1; fem and mog-1; fog-1 double mutants all make oocytes rather than sperm. Therefore, we propose that wild-type mog-1 is required in the hermaphrodite germ line for regulation of the switch from spermatogenesi s to oogenesis rather than for specification of oogenesis per se. In addition to its role in germline sex determination, maternal mog-1 is required for embryogenesis: most progeny of a mog-1; fem or mog-1; fog-1 mother die as embryos. How might the roles of mog-1 in the sperm/oocyte switch and embryogenesis be linked? Previous work showed that fem-3 is regulated post-transcrip tionally to achieve the sperm/oocyte switch. We speculate that mog-1 may function in the post-transcrip tional regulation of numerous germ-line RNAs, including fem-3. A loss of mog-1 might inappropriatel y activate fem-3 and thereby abolish the sperm/oocyte switch; its loss might also lead to misregulation of maternal RNAs and thus embryonic death.PL Graham, JE Kimble

    Source: Genetics, Vol. 133 (1993), pp. 919-931.

  4. The SL1 trans-spliced leader RNA performs an essential embryonic function in Caenorhabditis elegans that can also be supplied by SL2 RNA.: Genes and Development, Vol. 10 (1996), pp. 1543-1556.Cova lent joining of leader RNA exons to pre-mRNAs by trans-splicing has been observed in protists and invertebrates, and can occur in cultured mammalian cells. In the nematode Caenorhabditis elegans, approximately 60% of mRNA species are trans-spliced to the 22-nucleotide SL1 leader, and another approximately 10% of mRNAs receive the 22-nucleotide SL2 leader. We have isolated deletions that remove the rrs-1 cluster, a gene complex that contains approximately 110 tandem copies of a repeat encoding both SL1 RNA and 5S rRNA. An SL1-encoding gene alone rescues the embryonic lethality caused by these deletions. Mutations within the Sm-binding site of SL1 RNA, which is required for trans-splicing , eliminate rescue, suggesting that the ability of the SL1 leader to be trans-spliced is required for its essential activity. We observe pleiotropic defects in embryos lacking SL1 RNA, suggesting that multiple mRNAs may be affected by the absence of an SL1 leader. We found, however, that SL1-receiving messages are expressed without an SL1 leader. Surprisingly, when overexpressed, SL2 RNA, which performs a distinct function from that of SL1 RNA in wild-type animals, can rescue the lethality of embryos lacking SL1 RNA. Moreover, in these mutant embryos, we detect SL2 instead of SL1 leaders on normally SL1-trans-spli ced messages; this result suggests that the mechanism that discriminates between SL1 and SL2-trans-spli cing may involve competition between SL1 and SL2-specific trans-splicing . Our findings demonstrate that SL1 RNA is essential for embryogenesis in C. elegans and that SL2 RNA can substitute for SL1 RNA in vivo.KC Ferguson, PJ Heid, JH Rothman

    Source: Genes and Development, Vol. 10 (1996), pp. 1543-1556.

  5. Specification and development of the germline in Caenorhabditis elegans.: Ciba Foundation Symposium, Vol. 182 (1994), pp. 31-45.Maternal -effect sterile (mes) genes encode maternal components that are required for establishment and development of the germline. Five such genes have been identified in the nematode Caenorhabditis elegans. Mutations in one of the genes result in defects in the asymmetric division and cytoplasmic partitioning that generate the primordial germ cell P4 at the 16-24-cell stage of embryogenesis. As a result of these defects, the P4 cell is transformed into a muscle progenitor and mutant embryos develop into sterile adults with extra body muscles. Mutations in the other four mes genes do not affect formation of the germline during embryogenesis, but result in drastically reduced proliferation of the germline during post-embryonic stages and in an absence of gametes in adults. The failure to form gametes may reflect a defect in germline specification or may be a consequence of reduced germline proliferation. We are currently testing these two possibilities. In addition to the mes gene products, wild-type function of the zygotic gene glp-4 is required for normal post-embryonic proliferation of the germline. Germ cells in glp-4 mutant worms are arrested in prophase of the mitotic cell cycle and are unable to enter meiosis and form gametes. Thus, following establishment of the germ lineage in the early embryo, both maternal and zygotic gene products work in concert to promote the extensive proliferation of the germline and to enable germ cells to generate functional gametes.S Strome, CM Garvin, JE Paulsen, EE Capowski, PR Martin, MJ Beanan

    Source: Ciba Foundation Symposium, Vol. 182 (1994), pp. 31-45.

  6. Maternal depletion of CTCF reveals multiple functions during oocyte and preimplantatio n embryo development.: Development (Cambridge, England) (9 July 2008)CTCF is a multifunctiona l nuclear factor involved in epigenetic regulation. Despite recent advances that include the systematic discovery of CTCF-binding sites throughout the mammalian genome, the in vivo roles of CTCF in adult tissues and during embryonic development are largely unknown. Using transgenic RNAi, we depleted maternal stores of CTCF from growing mouse oocytes, and identified hundreds of misregulated genes. Moreover, our analysis suggests that CTCF predominantly activates or derepresses transcription in oocytes. CTCF depletion causes meiotic defects in the egg, and mitotic defects in the embryo that are accompanied by defects in zygotic gene expression, and culminate in apoptosis. Maternal pronuclear transfer and CTCF mRNA microinjection experiments indicate that CTCF is a mammalian maternal effect gene, and that persistent transcriptiona l defects rather than persistent chromosomal defects perturb early embryonic development. This is the first study detailing a global and essential role for CTCF in mouse oocytes and preimplantatio n embryos.Le-Ben Wan, Hua Pan, Sridhar Hannenhalli, Yong Cheng, Jun Ma, Andrew Fedoriw, Victor Lobanenkov, Keith E Latham, Richard M Schultz, Marisa S Bartolomei

    Source: Development (Cambridge, England) (9 July 2008)

  7. Structural differences in centromeric heterochromati n are spatially reconciled on fertilisation in the mouse zygote: Chromosoma, Vol. 116, No. 4. (August 2007), pp. 403-415.Probst , Aline, Santos, Fatima, Reik, Wolf, Almouzni, Genevieve, Dean, Wendy

    Source: Chromosoma, Vol. 116, No. 4. (August 2007), pp. 403-415.

  8. A maternal-zygot ic effect gene, Zfp57, maintains both maternal and paternal imprints.: Developmental cell, Vol. 15, No. 4. (October 2008), pp. 547-557.The mechanisms responsible for maintaining genomic methylation imprints in mouse embryos are not understood. We generated a knockout mouse in the Zfp57 locus encoding a KRAB zinc finger protein. Loss of just the zygotic function of Zfp57 causes partial neonatal lethality, whereas eliminating both the maternal and zygotic functions of Zfp57 results in a highly penetrant embryonic lethality. In oocytes, absence of Zfp57 results in failure to establish maternal methylation imprints at the Snrpn imprinted region. Intriguingly, methylation imprints are reacquired specifically at the maternally derived Snrpn imprinted region when the zygotic Zfp57 is present in embryos. This suggests that there may be DNA methylation-in dependent memory for genomic imprints. Zfp57 is also required for the postfertilizat ion maintenance of maternal and paternal methylation imprints at multiple imprinted domains. The effects on genomic imprinting are consistent with the maternal-zygot ic lethality of Zfp57 mutants.X Li, M Ito, F Zhou, N Youngson, X Zuo, P Leder, AC Ferguson-Smith

    Source: Developmental cell, Vol. 15, No. 4. (October 2008), pp. 547-557.

If you would like to find additional social bookmark based links on the topic of zygote we recommend the Open Tag Directory > Zygote. If you would like to find related tags we recommend Tag Patterns > Zygote.


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