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The Phenotype of Physcomitrium patens SMC6 Mutant with Interrupted Hinge Interactions

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61389030%3A_____%2F25%3A00639812" target="_blank" >RIV/61389030:_____/25:00639812 - isvavai.cz</a>

  • Alternative codes found

    RIV/00216224:14310/25:00144615

  • Result on the web

    <a href="https://doi.org/10.3390/genes16091091" target="_blank" >https://doi.org/10.3390/genes16091091</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.3390/genes16091091" target="_blank" >10.3390/genes16091091</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    The Phenotype of Physcomitrium patens SMC6 Mutant with Interrupted Hinge Interactions

  • Original language description

    Background/Objectives: nThe Structural Maintenance of Chromosomes (SMC) proteins form essential heterocomplexes for the preservation of DNA structure and its functions, and hence cell viability. The SMC5/6 dimer is assembled by direct interactions of ATP heads via the kleisin NSE4 bridge and by SMC hinges. The structure might be interrupted by a single point mutation within a conserved motif of the SMC6-hinge. We describe the phenomena associated with the impairment of the SMC5/6 complex with morphology, repair of DNA double strand breaks (DSB), mutagenesis, recombination and gene targeting (GT) in the moss Physcomitrium patens (P. patens). nMethods: nUsing CRISPR/Cas9-directed oligonucleotide replacement, we have introduced two close G to R point mutations in the hinge domain of SMC6 of P. patens and show that both mutations are not toxic and allow viability of mutant lines. nResults: nThe G514R mutation fully prevents the interaction of SMC6 not only with SMC5, but also with NSE5 and NSE6, while the mutation at G517R has no effect. The Ppsmc6_G514R line has aberrant morphology, spontaneous and bleomycin-induced mutagenesis, and maintenance of the number of rDNA copies. The most unique feature is the interference with gene targeting (GT), which is completely abolished. In contrast, the Ppsmc6_G517R line is close to WT in many aspects. Surprisingly, both mutations have no direct effect on the rate of DSB repair in dividing and differentiated cells. nConclusions: nAbolished interactions of SMC6 with SMC5 and NSE5,6 partners, which allow DSB repair, but impair other repair and recombination functions, suggests also regulatory role for SMC6.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    10603 - Genetics and heredity (medical genetics to be 3)

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2025

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    Genes

  • ISSN

    2073-4425

  • e-ISSN

    2073-4425

  • Volume of the periodical

    16

  • Issue of the periodical within the volume

    9

  • Country of publishing house

    CH - SWITZERLAND

  • Number of pages

    15

  • Pages from-to

    1091

  • UT code for WoS article

    001579980600001

  • EID of the result in the Scopus database

    2-s2.0-105017393204