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Truncating the spliceosomal 'rope protein' Prp45 results in Htz1 dependent phenotypes

Identifikátory výsledku

  • Kód výsledku v IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F60077344%3A_____%2F24%3A00603215" target="_blank" >RIV/60077344:_____/24:00603215 - isvavai.cz</a>

  • Nalezeny alternativní kódy

    RIV/00216208:11310/24:10487127

  • Výsledek na webu

    <a href="https://doi.org/10.1080/15476286.2024.2348896" target="_blank" >https://doi.org/10.1080/15476286.2024.2348896</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1080/15476286.2024.2348896" target="_blank" >10.1080/15476286.2024.2348896</a>

Alternativní jazyky

  • Jazyk výsledku

    angličtina

  • Název v původním jazyce

    Truncating the spliceosomal 'rope protein' Prp45 results in Htz1 dependent phenotypes

  • Popis výsledku v původním jazyce

    Spliceosome assembly contributes an important but incompletely understood aspect of splicing regulation. Prp45 is a yeast splicing factor which runs as an extended fold through the spliceosome, and which may be important for bringing its components together. We performed a whole genome analysis of the genetic interaction network of the truncated allele of PRP45 (prp45(1-169)) using synthetic genetic array technology and found chromatin remodellers and modifiers as an enriched category. In agreement with related studies, H2A.Z-encoding HTZ1, and the components of SWR1, INO80, and SAGA complexes represented prominent interactors, with htz1 conferring the strongest growth defect. Because the truncation of Prp45 disproportionately affected low copy number transcripts of intron-containing genes, we prepared strains carrying intronless versions of SRB2, VPS75, or HRB1, the most affected cases with transcription-related function. Intron removal from SRB2, but not from the other genes, partly repaired some but not all the growth phenotypes identified in the genetic screen. The interaction of prp45(1-169) and htz1 Delta was detectable even in cells with SRB2 intron deleted (srb2 Delta i). The less truncated variant, prp45(1-330), had a synthetic growth defect with htz1 Delta at 16 degrees C, which also persisted in the srb2 Delta i background. Moreover, htz1 Delta enhanced prp45(1-330) dependent pre-mRNA hyper-accumulation of both high and low efficiency splicers, genes ECM33 and COF1, respectively. We conclude that while the expression defects of low expression intron-containing genes contribute to the genetic interactome of prp45(1-169), the genetic interactions between prp45 and htz1 alleles demonstrate the sensitivity of spliceosome assembly, delayed in prp45(1-169), to the chromatin environment.

  • Název v anglickém jazyce

    Truncating the spliceosomal 'rope protein' Prp45 results in Htz1 dependent phenotypes

  • Popis výsledku anglicky

    Spliceosome assembly contributes an important but incompletely understood aspect of splicing regulation. Prp45 is a yeast splicing factor which runs as an extended fold through the spliceosome, and which may be important for bringing its components together. We performed a whole genome analysis of the genetic interaction network of the truncated allele of PRP45 (prp45(1-169)) using synthetic genetic array technology and found chromatin remodellers and modifiers as an enriched category. In agreement with related studies, H2A.Z-encoding HTZ1, and the components of SWR1, INO80, and SAGA complexes represented prominent interactors, with htz1 conferring the strongest growth defect. Because the truncation of Prp45 disproportionately affected low copy number transcripts of intron-containing genes, we prepared strains carrying intronless versions of SRB2, VPS75, or HRB1, the most affected cases with transcription-related function. Intron removal from SRB2, but not from the other genes, partly repaired some but not all the growth phenotypes identified in the genetic screen. The interaction of prp45(1-169) and htz1 Delta was detectable even in cells with SRB2 intron deleted (srb2 Delta i). The less truncated variant, prp45(1-330), had a synthetic growth defect with htz1 Delta at 16 degrees C, which also persisted in the srb2 Delta i background. Moreover, htz1 Delta enhanced prp45(1-330) dependent pre-mRNA hyper-accumulation of both high and low efficiency splicers, genes ECM33 and COF1, respectively. We conclude that while the expression defects of low expression intron-containing genes contribute to the genetic interactome of prp45(1-169), the genetic interactions between prp45 and htz1 alleles demonstrate the sensitivity of spliceosome assembly, delayed in prp45(1-169), to the chromatin environment.

Klasifikace

  • Druh

    J<sub>imp</sub> - Článek v periodiku v databázi Web of Science

  • CEP obor

  • OECD FORD obor

    10608 - Biochemistry and molecular biology

Návaznosti výsledku

  • Projekt

  • Návaznosti

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Ostatní

  • Rok uplatnění

    2024

  • Kód důvěrnosti údajů

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Údaje specifické pro druh výsledku

  • Název periodika

    RNA biology

  • ISSN

    1547-6286

  • e-ISSN

    1555-8584

  • Svazek periodika

    21

  • Číslo periodika v rámci svazku

    1

  • Stát vydavatele periodika

    GB - Spojené království Velké Británie a Severního Irska

  • Počet stran výsledku

    18

  • Strana od-do

    543-559

  • Kód UT WoS článku

    001237152800001

  • EID výsledku v databázi Scopus

    2-s2.0-85192166077