[
    {
        "id": "authors:whddq-2nr50",
        "collection": "authors",
        "collection_id": "whddq-2nr50",
        "cite_using_url": "https://resolver.caltech.edu/CaltechAUTHORS:20200629-073648893",
        "type": "article",
        "title": "Copulation defective mutants of C. elegans",
        "author": [
            {
                "family_name": "Hajdu-Cronin",
                "given_name": "Yvonne M.",
                "clpid": "Hajdu-Cronin-Y-M"
            },
            {
                "family_name": "Liu",
                "given_name": "Katharine S.",
                "clpid": "Liu-Katharine-S"
            },
            {
                "family_name": "Barber",
                "given_name": "Leslie",
                "clpid": "Barber-Leslie"
            },
            {
                "family_name": "Chamberlin",
                "given_name": "Helen M.",
                "clpid": "Chamberlin-H-M"
            },
            {
                "family_name": "Boorstein",
                "given_name": "William",
                "clpid": "Boorstein-W"
            },
            {
                "family_name": "Sternberg",
                "given_name": "Paul W.",
                "orcid": "0000-0002-7699-0173",
                "clpid": "Sternberg-P-W"
            }
        ],
        "abstract": "To identify genes involved in male copulatory behavior, we carried out an F2 clonal screen in a him-5 mutant background. We identified 20 mutations that affect male mating behavior without causing gross defects in morphology. \n\nMale mating in C. elegans comprises at least five steps (Liu and Sternberg, 1995). (l) The male responds to the hermaphrodite by backing his tail along the length of the hermaphrodite, (2) he turns over or under her body before reaching the head or tail, (3) he locates the vulva with his tail, at which point he stops backing, (4) he inserts his spicules into the vulva, and (5) he transfers sperm. To study the genetic basis for male mating behavior, we are isolating and characterizing Copulation Defective (Cod) mutations. We screened for mutant strains defective in this behavior using the screen described by Hodgkin (1983). him-5(e1490) worms are mutagenized with ethyl methane sulfonate (EMS); 20 P0 L4 hermaphrodites are picked singly to Petri plates; ten F1 worms are picked per mutagenized P0; and ten F2 L4 hermaphrodites are singled per P0 and their male progeny tested for mating efficiency via a qualitative mating test (six males crossed with six unc-52(e444) hermaphrodites, which are paralyzed at adulthood (Brenner, 1974). Mutants with phenotypes that are likely to reduce mating efficiency in a non-specific manner (such as those causing an Unc, Dpy, or Lon phenotype) were discarded. Those strains that appear morphologically normal under the dissecting microscope yet fail to mate or mate at a very low efficiency (1-5% cross progeny compared to wild type) were screened under Nomarski optics for defects in male reproductive structures. We screened over 3000 haploid genomes, and picked over 100 strains with reproduction defects. Nineteen strains were successfully backcrossed, which represents about 25% of the total strains attempted.  This result suggests that most strains harbor two or more mutations that contribute to the mating-deficiency defect. Preliminary analysis of behavior suggests that every major step in the wild-type mating pathway has at least one corresponding Cod mutation blocking the behavior, with several mutations blocking at the spicule insertion step. The screen also yielded morphological mutants, whose phenotypes include crumpled spicules, abnormal rays, and a gonad migration defect; some of these will be described elsewhere (Chamberlin &amp; Sternberg; micropublication in preparation).",
        "doi": "10.17912/W2XH3S",
        "pmcid": "PMC7255866",
        "issn": "2578-9430",
        "publisher": "Caltech Library",
        "publication": "microPublication Biology",
        "publication_date": "2017-11-02",
        "pages": "10.17912/W2XH3S"
    },
    {
        "id": "authors:a7ce1-1mh95",
        "collection": "authors",
        "collection_id": "a7ce1-1mh95",
        "cite_using_url": "https://resolver.caltech.edu/CaltechAUTHORS:20190514-112709230",
        "type": "article",
        "title": "Characterization of Seven Genes Affecting Caenorhabditis elegans Hindgut Development",
        "author": [
            {
                "family_name": "Chamberlin",
                "given_name": "Helen M.",
                "clpid": "Chamberlin-H-M"
            },
            {
                "family_name": "Brown",
                "given_name": "Keith B.",
                "clpid": "Brown-K-B"
            },
            {
                "family_name": "Sternberg",
                "given_name": "Paul W.",
                "orcid": "0000-0002-7699-0173",
                "clpid": "Sternberg-P-W"
            },
            {
                "family_name": "Thomas",
                "given_name": "James H.",
                "clpid": "Thomas-J-H"
            }
        ],
        "abstract": "We have identified and characterized 12 mutations in seven genes that affect the development of the Caenorhabditis elegans hindgut. We find that the mutations can disrupt the postembryonic development of the male-specific blast cells within the hindgut, the hindgut morphology in both males and hermaphrodites, and in some cases, the expression of a hindgut marker in hermaphrodite animals. Mutations in several of the genes also affect viability. On the basis of their mutant phenotypes, we propose that the genes fall into four distinct classes: (1) egl-5 is required for regional identity of the tail; (2) sem-4 is required for a variety of ectodermal and mesodermal cell types, including cells in the hindgut; (3) two genes, lin-49 and lin-59, affect development of many cells, including hindgut; and (4) three genes, mab-9, egl-38, and lin-48, are required for patterning fates within the hindgut, making certain hindgut cells different from others. We also describe a new allele of the Pax gene egl-38 that is temperature sensitive and affects the conserved \u03b2-hairpin of the EGL-38 paired domain. Our results suggest that a combination of different factors contribute to normal C. elegans hindgut development.",
        "pmcid": "PMC1460777",
        "issn": "0016-6731",
        "publisher": "Genetics Society of America",
        "publication": "Genetics",
        "publication_date": "1999-10-01",
        "series_number": "2",
        "volume": "153",
        "issue": "2",
        "pages": "731-742"
    },
    {
        "id": "authors:pdzcm-jr411",
        "collection": "authors",
        "collection_id": "pdzcm-jr411",
        "cite_using_url": "https://resolver.caltech.edu/CaltechAUTHORS:20120217-153949429",
        "type": "article",
        "title": "The lin-3/let-23 pathway mediates inductive signalling during male spicule development in Caenorhabditis elegans",
        "author": [
            {
                "family_name": "Chamberlin",
                "given_name": "Helen M.",
                "clpid": "Chamberlin-H-M"
            },
            {
                "family_name": "Sternberg",
                "given_name": "Paul W.",
                "orcid": "0000-0002-7699-0173",
                "clpid": "Sternberg-P-W"
            }
        ],
        "abstract": "During Caenorhabditis elegans male spicule development, four pairs of precursor cells respond to multiple positional cues and establish a pattern of fates that correlates with relative anterior-posterior cell position. One of the extracellular cues is provided by the F and U cells, which promote anterior fates. We show that the genes in the lin-3/let-23 signalling pathway required for hermaphrodite vulval induction also mediate this F/U signal. Reduction-of-function mutations in lin-3, let-23, sem-5, let-60 or lin-45 disrupt the fate of anterior cells. Likewise, activation of the pathway with ubiquitously produced signal results in posterior cells inappropriately adopting the anterior fates even in the absence of F and U. We have further used this genetic pathway to begin to understand how multiple positional cues are integrated to specify cell fate. We demonstrate that lin-15 acts in spicule development as it does in vulval induction, as a negative regulator of let-23 receptor activity. A second extracellular cue, from Y.p, also acts antagonistically to the lin-3/let-23 pathway. However, this signal is apparently integrated into the lin-3/let-23 pathway at some step after lin-45 raf and is thus functionally distinct from lin-15. We have also investigated the role of lin-12 in forming the anterior/posterior pattern of fates. A lin-12 gain-of-function defect is masked by redundant positional information from F and U.",
        "issn": "0950-1991",
        "publisher": "Company of Biologists",
        "publication": "Development",
        "publication_date": "1994-10",
        "series_number": "10",
        "volume": "120",
        "issue": "10",
        "pages": "2713-2721"
    },
    {
        "id": "authors:jqge3-g2293",
        "collection": "authors",
        "collection_id": "jqge3-g2293",
        "cite_using_url": "https://resolver.caltech.edu/CaltechAUTHORS:20120229-094019491",
        "type": "article",
        "title": "Multiple cell interactions are required for fate specification during male spicule development in Caenorhabditis elegans",
        "author": [
            {
                "family_name": "Chamberlin",
                "given_name": "Helen M.",
                "clpid": "Chamberlin-H-M"
            },
            {
                "family_name": "Sternberg",
                "given_name": "Paul W.",
                "orcid": "0000-0002-7699-0173",
                "clpid": "Sternberg-P-W"
            }
        ],
        "abstract": "The B blast cell divides postembryonically in C. elegans males to produce 47 progeny that include all of the cells of the copulatory spicules. During the early development of the B lineage, the anterior daughter of B, B.a, generates eight cells. These cells migrate to form four pairs of cells that flank the developing cloaca (ventral, dorsal, and two identical lateral pairs). For each pair, the more anterior cell produces a distinct lineage ('anterior fate') from the posterior cell ('posterior fate'). For the ventral and dorsal pairs, either cell can migrate to the anterior position and produce the anterior lineage, and the other cell migrates posterior and produces the posterior lineage (Sulston and Horvitz, 1977, Dev. Biol. 56, 110\u2013156). The migration is variable, although the resultant fate pattern is invariant. In the two lateral pairs, both the migration and fate pattern are invariant. Using a laser microbeam to selectively ablate neighboring cells we have found that the cells of the lateral pair also respond to positional cues. For all four pairs other male-specific blast cells provide extracellular cues. In general, F and U promote anterior fates, Y promotes some posterior fates, and the B.a progeny promote posterior fates. Several of these cues are redundant. By ablating combinations of cells we have deduced how these signals may act in concert to specify the fates of the B.a progeny. We propose that fate specification in these pairs depends on three general classes of extracellular cues: positional cues, modulators of positional cues, and lateral signals. The B lineage thus provides an opportunity to study with single cell resolution the integration of multiple intercellular signals.",
        "issn": "0950-1991",
        "publisher": "Company of Biologists",
        "publication": "Development",
        "publication_date": "1993-06",
        "series_number": "2",
        "volume": "118",
        "issue": "2",
        "pages": "297-324"
    }
]