[
    {
        "id": "authors:vtc0n-pnz59",
        "collection": "authors",
        "collection_id": "vtc0n-pnz59",
        "cite_using_url": "https://resolver.caltech.edu/CaltechAUTHORS:20170408-205519929",
        "type": "article",
        "title": "Dual functions of the Drosophila eyes absent gene in the eye and embryo",
        "author": [
            {
                "family_name": "Leiserson",
                "given_name": "William M.",
                "clpid": "Leiserson-W-M"
            },
            {
                "family_name": "Benzer",
                "given_name": "Seymour",
                "clpid": "Benzer-S"
            },
            {
                "family_name": "Bonini",
                "given_name": "Nancy M.",
                "clpid": "Bonini-N-M"
            }
        ],
        "abstract": "In eyes absent (eya) mutants, eye progenitor cells undergo cell death early in development. Whereas the phenotype of eya1 is limited to the eye, other mutations are lethal. Genetic and molecular analysis reveals that mutations in one region of the gene cause embryonic lethality, whereas mutations throughout the gene cause defects in eye development. Mosaic analysis indicates that the eya requirement is cell autonomous. In eye-specific mutants, expression in the eye disc is lacking while embryonic expression is normal. Both the type I and type II transcripts are expressed in the developing eye, and expression of either can rescue the eye phenotype. These data indicate a specific requirement for eya function in eye progenitor cells that is normally fulfilled by both transcripts.",
        "doi": "10.1016/S0925-4773(98)00052-5",
        "issn": "0925-4773",
        "publisher": "Elsevier",
        "publication": "Mechanisms of Development",
        "publication_date": "1998-05",
        "series_number": "2",
        "volume": "73",
        "issue": "2",
        "pages": "193-202"
    },
    {
        "id": "authors:dx7y6-s4c93",
        "collection": "authors",
        "collection_id": "dx7y6-s4c93",
        "cite_using_url": "https://resolver.caltech.edu/CaltechAUTHORS:20190227-144139135",
        "type": "article",
        "title": "Multiple Roles of the eyes absent Gene in Drosophila",
        "author": [
            {
                "family_name": "Bonini",
                "given_name": "Nancy M.",
                "clpid": "Bonini-N-M"
            },
            {
                "family_name": "Leiserson",
                "given_name": "William M.",
                "clpid": "Leiserson-W-M"
            },
            {
                "family_name": "Benzer",
                "given_name": "Seymour",
                "clpid": "Benzer-S"
            }
        ],
        "abstract": "Theeyes absent(eya) gene plays an essential role in the events that lead to formation of theDrosophilaeye; without expression ofeyain retinal progenitor cells, they undergo programmed cell death just prior to the morphogenetic furrow, leading to an eyeless or reduced eye phenotype. Theeyagene has recently been found to be highly conserved to humans, defining a new gene family. Insights into the gene's function in the fly, therefore, are likely to be relevant to the role of its homologs in vertebrates. Detailed studies at the subcellular level indicate that the Eya protein is localized to the nucleoplasm, suggesting a role in control of nuclear events. Theeyagene shows expression and roles in tissues other than the eye, including subsets of cells of the adult visual system, brain, and ovary, as well as an elaborate expression pattern in the embryo. Various mutations in theeyagene cause loss of ocelli, female sterility, or lethality. Analysis of the embryonic lethal phenotype indicates that mutant alleles show defects in head morphogenesis. These data indicate thateyahas critical roles in morphogenesis of a number of tissues in the animal, in addition to its role in early eye formation. Despite multiple roles at multiple stages of development of the fly, both the type I and type II forms of the protein, when expressed ectopically during larval development, can direct eye formation.",
        "doi": "10.1006/dbio.1997.8845",
        "issn": "0012-1606",
        "publisher": "Elsevier",
        "publication": "Developmental Biology",
        "publication_date": "1998-04-01",
        "series_number": "1",
        "volume": "196",
        "issue": "1",
        "pages": "42-57"
    },
    {
        "id": "authors:x5a2h-mn708",
        "collection": "authors",
        "collection_id": "x5a2h-mn708",
        "cite_using_url": "https://resolver.caltech.edu/CaltechAUTHORS:20190227-112246122",
        "type": "article",
        "title": "Transvection at the eyes absent gene of Drosophila",
        "author": [
            {
                "family_name": "Leiserson",
                "given_name": "William M.",
                "clpid": "Leiserson-W-M"
            },
            {
                "family_name": "Bonini",
                "given_name": "Nancy M.",
                "clpid": "Bonini-N-M"
            },
            {
                "family_name": "Benzer",
                "given_name": "Seymour",
                "clpid": "Benzer-S"
            }
        ],
        "abstract": "The Drosophila eyes absent (eya) gene is required for survival and differentiation of eye progenitor cells. Loss of gene function in the eye results in reduction or absence of the adult compound eye. Certain combinations of eya alleles undergo partial complementation, with dramatic restoration of eye size. This interaction is sensitive to the relative positions of the two alleles in the genome; rearrangements predicted to disrupt pairing of chromosomal homologs in the eya region disrupt complementation. Ten X-ray-induced rearrangements that suppress the interaction obey the same general rules as those that disrupt transvection at the bithorax complex and the decapentaplegic gene. Moreover, like transvection in those cases, the interaction at eya depends on the presence of normal zeste function. The discovery of transvection at eya suggests that transvection interactions of this type may be more prevalent than generally thought.",
        "pmcid": "PMC1206256",
        "issn": "0016-6731",
        "publisher": "Genetics Society of America",
        "publication": "Genetics",
        "publication_date": "1994-12-01",
        "series_number": "4",
        "volume": "138",
        "issue": "4",
        "pages": "1171-1179"
    },
    {
        "id": "authors:t71vj-2ec21",
        "collection": "authors",
        "collection_id": "t71vj-2ec21",
        "cite_using_url": "https://resolver.caltech.edu/CaltechAUTHORS:20190228-115826749",
        "type": "article",
        "title": "The eyes absent gene: Genetic control of cell survival and differentiation in the developing Drosophila eye",
        "author": [
            {
                "family_name": "Bonini",
                "given_name": "Nancy M.",
                "clpid": "Bonini-N-M"
            },
            {
                "family_name": "Leiserson",
                "given_name": "William M.",
                "clpid": "Leiserson-W-M"
            },
            {
                "family_name": "Benzer",
                "given_name": "Seymour",
                "clpid": "Benzer-S"
            }
        ],
        "abstract": "The eyes absent (eya) gene is required at an early stage in development of the D. melanogaster compound eye. In eya mutants, progenitor cells in the eye disc undergo programmed cell death anterior to the morphogenetic furrow, rather than proceeding into the pathway of retinal differentiation. A low level of cell death normally occurs at this stage, suggesting that eya activity influences the distribution of cells between differentiation and death. Molecular analysis identifies a nuclear protein expressed in progenitor cells prior to differentiation. Transformation with the cDNA prevents progenitor cell death and allows the events that generate the eye to proceed. eya activity is required for the survival of eye progenitor cells at a critical stage in morphogenesis.",
        "doi": "10.1016/0092-8674(93)90115-7",
        "issn": "0092-8674",
        "publisher": "Elsevier",
        "publication": "Cell",
        "publication_date": "1993-02-12",
        "series_number": "3",
        "volume": "72",
        "issue": "3",
        "pages": "379-395"
    }
]