Seven temperature-sensitive cell lysis (cy) mutant strains of Saccharomyces cerevisiae were isolated which lyse at the restrictive temperature on hypotonic but not on osmotically supported medium. The seven mutants fell into four complementation groups, CLY12 to CLY15. The wild-type CLY1S gene was isolated by complementation of the clyl5 temperature-sensitive growth defect. Sequence analysis revealed that the complementing DNA fragment encoded a partial PKC1 gene, which has previously been isolated as an S. cerevisiae homolog of mammalian protein kinase C genes (D. E. Levin, F. 0. Fields, R. Kunisawa, J. M. Bishop, and J. Thorner, Cell 62:213-224, 1990 The yeast cell wall is a complex rigid structure, responsible for cell shape, which undergoes a series of significant changes during the mitotic cell cycle (6). For example, bud emergence requires modifications of the cell wall at a precisely localized site and controlled cell wall growth in order to produce a daughter cell. Other cellular processes such as mating and sporulation also involve specific alterations of the cell wall structure.Yeast cell walls are constructed almost entirely of two classes of polysaccharides: polymers of mannose covalently linked to peptides, which are termed mannoproteins, and polymers of glucose, termed glucans. A third sugar polymer of N-acetylglucosamine, chitin, is present in only minor amounts (8). A number of Saccharomyces cerevisiae mutants with defects in the synthesis of cell wall components have been isolated. Defects in agglutination with a 1,3-alinked mannose antiserum define mannoprotein (mnn) mutants (reviewed in Ballou [1]), yeast killer toxin-resistant (kre) mutants display reduced levels of 1,6-,-glucan in the cell wall (2), and chitin synthase mutants are unable to convert exogenous glucosamine to chitin (3,22). The major cell wall-degrading enzyme activities mainly consist of 1,3-,-and

The SDB23 gene of Saccharomyces cerevisiae was isolated in a search for high copy‐number suppressors of mutations in a cell cycle gene, DBF2, SDB23 encodes a 21,276 Da protein with significant sequence similarity to characterized mammalian snRNP core proteins. Examination of multiple sequence alignments of snRNP core proteins with Sdb23p indicates that all of these proteins share a number of highly conserved residues, and identifies a novel motif for snRNP core proteins. Sdb23p is essential for cell viability and is required for nuclear pre‐mRNA splicing both in vivo and in vitro. Extracts prepared from Sdb23p‐depleted cells are unable to support splicing and have vastly reduced levels of U6 snRNA. The stability of U1, U2, U4 and U5 spliceosomal snRNAs is not affected by the loss of Sdb23p. Antibodies raised against Sdb23p strongly coimmunoprecipitate free U6 snRNA and U4/U6 base‐paired snRNAs. These results establish that SDB23 encodes a novel U6 snRNA‐associated protein that is essential for the stability of U6 snRNA. We therefore propose the more logical name USS1 (U‐Six SnRNP) for this gene.

Suicide rates among American Indian youth in the United States are two to three times the national average. Risk factors for American Indian youth include depression, alcohol use, hopelessness and stress, and family conflict, abuse, poverty, and instability. In this descriptive study, the authors aimed to obtain parents' and elders' perspectives on community needs and to identify strengths on which the community might build to reduce youth suicide risk. Data were collected from focus groups with 40 American Indian parents and from individual interviews with 9 American Indian elders. The major task participants addressed was holding the family together and healing intergenerational pains. Topics parents discussed were holding onto cultural values, holding the family together, getting through school, and getting a job. These findings substantiate previous research and provide useful information for the design of culturally appropriate family or community-based interventions to prevent American Indian youth suicide.

Using a DNA fragment derived from the Saccharomyces cerevisiae protein kinase C gene (PKC1) as a probe to screen an ordered array library of genomic DNA from the dimorphic pathogenic fungus Candida albicans, the C. albicans PKC1 gene (CaPKC1) was isolated. The CaPKC1 gene is predicted to encode a protein of 1079 amino acids with 51% sequence identity over the entire length with the S. cerevisiae Pkc1 protein and is capable of functionally complementing the growth defects of a S. cerevisiae pkc1Δ mutant strain on hypo‐osmotic medium. Deletion of both endogenous copies of the CaPKC1 gene in diploid C. albicans cells resulted in an osmotically remedial cell lysis defect of both the budding and the hyphal growth form and morphologically aberrant cells of the budding form. Despite these abnormalities, the transition between the two growth forms of C. albicans occurred normally in pkc1/pkc1 double disruptants. Capkc1p was modified at its C‐terminus with two repeats of the Staphylococcus aureus protein A IgG‐binding fragment (ZZ‐sequence tag) and partially purified by chromatography on DEAE–Sepharose and IgG–Sepharose. In vitro, Capkc1p preferably phosphorylated the S. cerevisiae Pkc1p pseudosubstrate peptide and myelin basic protein, but not histones, protamine or dephosphorylated casein, and failed to respond to cofactors known to activate several mammalian PKC isozymes.

This is an open access article under the terms of the Creat ive Commo ns Attri bution-NonCo mmerc ial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. Abstract Introduction: Expanding access to postpartum intrauterine contraception (PPIUC) can reduce unintended pregnancies and short inter-pregnancy intervals; however, provision across Europe is limited. Our aim was to determine the feasibility, clinical outcomes and patient satisfaction of providing immediate PPIUC after vaginal birth using a health services research model. Material and methods: Phased introduction of PPIUC across two Lothian maternity hospitals; all women intending vaginal birth during the study period without a contraindication to use of the method were eligible to receive PPIUC. Midwives and obstetric doctors were trained in vaginal PPIUC insertion using Kelly forceps. Women received information antenatally and had PPIUC insertion of either a levonorgestrel intrauterine system or a copper intrauterine device within 48 hours of vaginal birth.Follow-up was conducted in-person at 6 weeks postpartum and by telephone at 3, 6 and 12 months. Primary outcomes were: uptake, complications (infection, uterine perforation), expulsion and patient satisfaction at 6 weeks; and method of continuation up to 12 months. Secondary outcomes included hazard ratio for expulsion adjusted for demographic and insertion-related variables.Results: Uptake of PPIUC was 4.6% of all vaginal births; 465/447 (96.1%) of those requesting PPIUC successfully received it and most chose a levonorgestrel intrauterine system (73%). At 6 weeks postpartum, the infection rate was 0.8%, there were no perforations and 98.3% of women said they would recommend the service. The complete expulsion rate was 29.8% (n = 113) and most had symptoms (n = 79). Of the additional 121 devices removed, 118 were because of partial expulsion. The rate of complete/partial expulsion was higher for insertions by midwives compared with those by doctors. The re-insertion rate after expulsion/removal was 87.6% and method continuation at 12 months was 79.6%. | 599COOPER Et al.