Publications
20 results found
Lawrence N, Dearden P, Hartley D, et al., 2000, dTcf antagonises Wingless signalling during the development and patterning of the wing in Drosophila, INTERNATIONAL JOURNAL OF DEVELOPMENTAL BIOLOGY, Vol: 44, Pages: 749-756, ISSN: 0214-6282
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- Citations: 14
Hartley D, 1996, Drosophila inherit diseases, NATURE GENETICS, Vol: 13, Pages: 133-134, ISSN: 1061-4036
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- Citations: 5
TATA F, HARTLEY DA, 1995, INHIBITION OF CELL FATE IN DROSOPHILA BY ENHANCER OF SPLIT GENES, MECHANISMS OF DEVELOPMENT, Vol: 51, Pages: 305-315, ISSN: 0925-4773
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- Citations: 51
BROWN NH, HARTLEY DA, 1994, DROSOPHILA DEVELOPMENT - EXPLORING SIGNALING PATHWAYS, NATURE, Vol: 370, Pages: 414-415, ISSN: 0028-0836
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- Citations: 2
TATA F, HARTLEY DA, 1993, THE ROLE OF THE ENHANCER OF SPLIT COMPLEX DURING CELL FATE DETERMINATION IN DROSOPHILA, DEVELOPMENT, Pages: 139-148, ISSN: 0950-1991
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- Citations: 26
DELIDAKIS C, PREISS A, HARTLEY DA, et al., 1991, 2 GENETICALLY AND MOLECULARLY DISTINCT FUNCTIONS INVOLVED IN EARLY NEUROGENESIS RESIDE WITHIN THE ENHANCER OF SPLIT LOCUS OF DROSOPHILA-MELANOGASTER, GENETICS, Vol: 129, Pages: 803-823, ISSN: 0016-6731
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- Citations: 127
PREISS A, HARTLEY D, DELIDAKIS C, 1991, TOWARDS AN UNDERSTANDING OF E(SPL) NEUROGENIC FUNCTION, JOURNAL OF NEUROGENETICS, Vol: 7, Pages: 141-141, ISSN: 0167-7063
Artavanis-Tsakonas S, Delidakis C, Fehon R, et al., 1990, Notch and the molecular genetics of neuroblast segregation in Drosophila., Mol Reprod Dev, Vol: 27, Pages: 23-27, ISSN: 1040-452X
HARTLEY D, WHITE R, 1990, DROSOPHILA IN CRETE - A FLYING VISIT, TRENDS IN GENETICS, Vol: 6, Pages: 199-201, ISSN: 0168-9525
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- Citations: 3
Hartley DA, 1990, Early neurogenesis., Semin Cell Biol, Vol: 1, Pages: 185-196, ISSN: 1043-4682
After the symmetry of the early embryo is disrupted by morphogenetic movements, one of the first differentiation events is the appearance of discrete neural precursors, the neuroblasts, which segregate from a defined region of ectoderm. Within this region, presumptive epidermal precursors are intermingled with the neuroblasts. Sorting between these fates appears to depend upon cell-cell interactions and requires the function of two sets of genes; one whose mutant phenotype results in an excessive central nervous system (CNS) and the other a subnormal CNS. Molecular cloning of these genes reveals striking homologies which can place the products into two camps. The first are recognizable cell surface components (and potential signal transducers), and the second DNA binding proteins, plausibly transcription factors.
Rothberg JM, Hartley DA, Walther Z, et al., 1988, slit: an EGF-homologous locus of D. melanogaster involved in the development of the embryonic central nervous system., Cell, Vol: 55, Pages: 1047-1059, ISSN: 0092-8674
A family of loci homologous to the EGF-like portion of Notch, a gene involved in neurogenesis, have been identified in D. melanogaster. The sequence, spatial, and temporal distribution of both RNA and protein of one of these loci suggest a possible role in the development of the central nervous system (CNS). In situ hybridization and antibody staining of embryos show initial localization in cells along the midline of the neuroepithelium. High level expression is restricted in the developing embryo to a subset of six midline glial cells abutting growing axons. Extracellular localization is suggested by the presence of EGF-like repeats in the deduced protein sequence and antibody staining. Cytological, immunocytochemical, genetic, and molecular data show that this gene corresponds to the slit locus. Mutations in this locus result in the collapse of the regular scaffold of commissural and longitudinal axon tracts in the embryonic central nervous system.
Hartley DA, Preiss A, Artavanis-Tsakonas S, 1988, A deduced gene product from the Drosophila neurogenic locus, enhancer of split, shows homology to mammalian G-protein beta subunit., Cell, Vol: 55, Pages: 785-795, ISSN: 0092-8674
The correct segregation of neural from epidermal lineages in Drosophila embryogenesis depends on the activity of the six zygotic "neurogenic" genes. One of the neurogenic genes, Enhancer of split, is particularly noteworthy in its genetic interactions with Notch and Delta, which both appear to code for transmembrane proteins with homology to the epidermal growth factor. Transformation experiments have demonstrated the cloning of sequences necessary for Enhancer of split gene function. We report here that the gene product derived from DNA sequencing shows homology to the beta subunit of mammalian G proteins and CDC4, a yeast cell cycle gene. We demonstrate that expression of the transcripts relates to the developing central nervous system. These data suggest a mechanism of interaction between the gene products of Notch and Enhancer of split.
Preiss A, Hartley DA, Artavanis-Tsakonas S, 1988, The molecular genetics of Enhancer of split, a gene required for embryonic neural development in Drosophila, EMBO Journal, Vol: 7, Pages: 3917-3927
Hartley DA, Xu TA, Artavanis-Tsakonas S, 1987, The embryonic expression of the Notch locus of Drosophila melanogaster and the implications of point mutations in the extracellular EGF-like domain of the predicted protein., EMBO J, Vol: 6, Pages: 3407-3417, ISSN: 0261-4189
The Notch locus of Drosophila melanogaster is one of a small number of zygotically acting 'neurogenic' genes necessary for the correct segregation of neural from epidermal lineages during embryogenesis. The predicted gene product is implicated in a cell interaction mechanism required to achieve this ectodermal differentiation. We have examined wild-type Notch expression by in situ hybridization and find it to be expressed in more cells than we would have predicted given a sole function in regulating neurogenesis. We conclude from these data that Notch plays a more general role in development. In order to assess the dependence of Notch expression on other neurogenic gene function we have hybridized Notch probes to Enhancer of split mutants which are known to interfere with expression of Notch phenotypes. We intimate that the nature of interaction between these genes is not at the level of transcription. Instead, the DNA sequence of split, which is a missense mutation in the EGF-like extracellular domain of the Notch protein, suggests a direct biochemical interaction between Notch and E(spl) proteins. The similar site of a second point mutation, AxE2, implies that protein interactions also occur between Notch proteins. Finally we discuss the general implications of our findings with a view to the models and mechanisms of Notch action in regulating individual cellular interactions during development.
Hartley DA, Xu T, Artavanis-Tsakonas S, 1987, The embryonic expression of the Notch locus of Drosophila melanogaster and the implications of point mutations in the extracellular EGF-like domain of the predicted protein, EMBO Journal, Vol: 7, Pages: 3917-3927
NALBANTOGLU J, HARTLEY D, PHEAR G, et al., 1986, SPONTANEOUS DELETION FORMATION AT THE APRT LOCUS OF HAMSTER-CELLS - THE PRESENCE OF SHORT SEQUENCE HOMOLOGIES AND DYAD SYMMETRIES AT DELETION TERMINI, EMBO JOURNAL, Vol: 5, Pages: 1199-1204, ISSN: 0261-4189
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- Citations: 155
Hartley DA, Davies KE, Drayna D, et al., 1984, A cytological map of the human X chromosome - evidence for non-random recombination, Nucleic Acids Research, Vol: 12, Pages: 5277-5285
Drayna D, Davies KE, Hartley D, et al., 1984, Genetic mapping of the human X chromosome by using restriction fragment length polymorphisms, Proceedings of the National Academy of Sciences, Vol: 81, Pages: 2836-2839
Harper K, Winter RW, Pembrey ME, et al., 1984, A clinically useful DNA probe closely linked to haemophilia, Lancet, Vol: ii, Pages: 6-8
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