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Twentieth Fungal Genetics Conference Scientific Program Fungal Genetics Reports Volume 46 Article 19 Twentieth Fungal Genetics Conference Scientific Program Fungal Genetics Conference Follow this and additional works at: https://newprairiepress.org/fgr This work is licensed under a Creative Commons Attribution-Share Alike 4.0 License. Recommended Citation Fungal Genetics Conference. (1999) "Twentieth Fungal Genetics Conference Scientific Program," Fungal Genetics Reports: Vol. 46, Article 19. https://doi.org/10.4148/1941-4765.1247 This Supplementary Material is brought to you for free and open access by New Prairie Press. It has been accepted for inclusion in Fungal Genetics Reports by an authorized administrator of New Prairie Press. For more information, please contact [email protected]. Twentieth Fungal Genetics Conference Scientific Program Abstract Abstracts are published as an electronic supplement to Fungal Genetics Newsletter # 46 and should be cited as follows: Fungal Genet. Newsl. 46S: Abstract Number This supplementary material is available in Fungal Genetics Reports: https://newprairiepress.org/fgr/vol46/iss1/19 : Twentieth Fungal Genetics Conference Scientific Program TWENTIETH FUNGAL GENETICS CONFERENCE SCIENTIFIC PROGRAM • Plenary session abstracts • Regulation of Gene Expression (#s 1-124) • Sexual and Asexual Differentiation (#s 125-196) • Secondary Metabolism and Pathogenicity (#s 197-287) • Cell Biology (#s 288-379) • Unclassified (#s >380) Abstracts are published as an electronic supplement to Fungal Genetics Newsletter # 46 and should be cited as follows: Fungal Genet. Newsl. 46S: Abstract Number Plenary session abstracts • Session I: REGULATION OF GENE EXPRESSION • Session II: SEXUAL AND ASEXUAL DIFFERENTIATION • Session III: SECONDARY METABOLISM AND PATHOGENICITY • Session IV: CELL BIOLOGY Session I: REGULATION OF GENE EXPRESSION Chair: Eric Selker Vegetative incompatibility in Podospora anserina, characterization of genes induced during non-allelic incompatibility. Joël Bégueret, Institut CNRS de Biochimie et Génétique Cellulaires, Bordeaux, France. In P. anserina, nine het loci have been identified by genetic analysis of wild-type isolates. Five of these loci are involved in allelic incompatibility systems as described in Neurospora. crassa and other fungi. However in Podospora, genetic interactions between non-allelic het genes have also been described. In these cases, the incompatibility reaction is triggered by the coexpression of het genes that belong to different loci. Five het genes involved in such non-allelic incompatibility systems have been identified, they define three incompatibility systems, het- R/het-V, het-C/het-E and het-C/het-D. We have used the thermosensitivity of the het-R/het-V system to identified genes whose expression is induced during the progress of the incompatibility Published by New Prairie Press, 2017 1 Fungal Genetics Reports, Vol. 46 [1999], Art. 19 reaction. Four genes, named idi (for induced during incompatibility) have been characterized. idi-1, 2 and 3 encode small polypeptides that contain a signal peptide. Using GFP labelling, the idi-1p was found to be located in the septa. idi-4 encodes a transcription factor containing a b- ZIP domain. The expresion of pspA, a gene coding for a subtilisine-like protease is also highly enhanced during incompatibility. We observed that the expression of most of these genes is also induced when incompatibility is released by the other non-allelic incompatibility system, het- C/het-E, but not by the allelic system het-s/het-S. Some of these genes are also induced under glucose and/or nitrogen starvation suggesting a functional relationship between the cell death reaction induced during starvation or by the coexpression of non-allelic het genes. Translational control of gene expression. Matthew S. Sachs, Department of Biochemistry and Molecular Biology, Oregon Graduate Institute, Portland OR 97291-1000. Short peptide coding regions (upstream open reading frames or uORFs) in the 5'-leaders of eukaryotic mRNAs can serve critical regulatory functions. uORFs are found in many mRNAs in filamentous fungi. A single uORF with an evolutionarily conserved peptide sequence is found upstream of the structural genes for the small subunit of arginine-specific carbamoyl phosphate synthetase from Neurospora crassa, Magnaporthe grisea, Trichoderma virens, Aspergillus nidulans and Saccharomyces cerevisiae. The N. crassa uORF specifies a 24-residue peptide named the arginine attenuator peptide (AAP) because it is involved in negative, Arg-specific translational regulation. In vivo, the N. crassa AAP down-regulates translation of ARG2 in response to Arg by reducing the average number of ribosomes associated with the arg-2 mRNA. AAP-mediated translational regulation has been reconstituted in an N. crassa cell-free translation system. A primer extension inhibition assay has been used to map the positions of ribosomes on capped and polyadenylated synthetic RNAs added to this system. Arg causes ribosomes to stall soon after they have translated the AAP. Arg-specific ribosome stalling is proposed to result in Arg-specific negative regulation because such ribosomes would block ribosomal scanning from the 5'-end of the mRNA and therefore block trailing ribosomes from translating ARG2. The AAP amino acid sequence, but not the RNA sequence encoding it, is critical for regulation. AAP translation can cause stalling of ribosomes involved in termination or elongation. Regulation by these evolutionarily conserved fungal leader peptides represent a novel mechanism of cis-acting translational control. Chromatin modulation and regulation of pathogenic development in the smut fungus Ustilago maydis. Joerg T. Kaemper, Michael Reichmann, Claudia Quadbeck-Seeger, and Regine Kahmann. Ludwig-Maximilian-University, Genetics, Munich, Bavaria, Germany. In the phytopathogenic fungus Ustilago maydis the multiallelic b mating-type locus represents the central control locus for sexual and pathogenic development. The b locus encodes a pair of unrelated homeodomain proteins termed bE and bW that form heterodimers when originating from different alleles; the heterodimer is presumed to regulate pathogenicity genes, either directly by binding to cis regulatory sequences (class 1 genes), or indirectly via a b-dependent signal cascade (class 2 genes). Using a bE/bW fusion protein we were able to isolate the first direct target for the bE/bW heterodimer in the promoter of lga2, a gene located in the a locus. https://newprairiepress.org/fgr/vol46/iss1/19 DOI: 10.4148/1941-4765.1247 2 : Twentieth Fungal Genetics Conference Scientific Program This sequence is bound by the bE/bW heterodimer and mediates the b-dependent regulation of the gene in vivo. In a screen for components of the b-dependent signal cascade we have isolated two different genes, one coding for a histone deacetylase (Hda1), the other one for a protein (Rum1) with similarities to the human retinoblastoma binding protein 2. Both genes are essential for the establishment of a repressed state of several class 2 genes in the absence of the b heterodimer. We propose that both Hda1 and Rum1 are in a complex with other proteins with at least one of them allowing sequence specific DNA binding. In this model, the regulation of gene activity is achieved by modulation of the chromatine structure mediated by the action of the histone deacetylase Hda1. Genome defense in Neurospora. Eric Selker, Joseph Dobosy, Michael Freitag, Shan Hays, Greg Kothe, Elena Kuzminova, Brian Margolin, Johanna Swanson and Hisashi Tamaru. Institute of Molecular Biology, University of Oregon, Eugene, OR 97405. We wish to identify the important features of eukaryotic genomes and the forces responsible for shaping them. In organisms with small genomes, such as fungi, a large fraction of their DNA appears functional and may be maintained by natural selection alone. Even small genomes, however, are littered with sequences that look like selfish DNA. Although it is difficult to demonstrate that a particular sequence is useless, mechanisms well suited to fight selfish DNA have been found suggesting that genome structure is important. Neurospora has at least three distinct, but somewhat interrelated gene silencing systems that probably serve in genome defense: 1. RIP and RIP-associated methylation, 2. quelling, and 3. RIP-independent methylation of "foreign" DNA. We are using several approaches to investigate the control and mechanism of gene silencing systems - most particularly DNA methylation. One involves identification and characterization of mutants defective in methylation (dim). So far, we have identified four dim genes. Mutation of dim-2, which encodes a DNA methyltransferase, eliminates all methylation in vegetative cells and can derepress the transcription of some sequences and repress others. In the cases examined so far, methylation interferes with transcription elongation without affecting initiation. We have detected Neurospora proteins that bind to methylated sequences and may mediate these effects, potentially by influencing chromatin structure. Methylation-dependent silencing can be relieved by Trichostatin A (TSA), an inhibitor of histone deacetylases. Selective loss of methylation is associated with TSA treatment, suggesting that acetylation of chromatin proteins can directly or indirectly control DNA methylation. To explore the connection between DNA methylation and chromatin we are testing the effects of mutations in genes for histones H2A, H2B, H3, H4 and H1 and other candidate components of the
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