1. Chromosomes and Gene Expression
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Centromere deletion in Cryptococcus deuterogattii leads to neocentromere formation and chromosome fusions

  1. Klaas Schotanus
  2. Joseph Heitman  Is a corresponding author
  1. Duke University Medical Center, United States
Research Article
  • Cited 2
  • Views 1,047
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Cite this article as: eLife 2020;9:e56026 doi: 10.7554/eLife.56026

Abstract

The human fungal pathogen Cryptococcus deuterogattii is RNAi-deficient and lacks active transposons in its genome. C. deuterogattii has regional centromeres that contain only transposon relics. To investigate impact of centromere loss on the C. deuterogattii genome, either centromere 9 or 10 was deleted. Deletion of either centromere resulted in neocentromere formation and interestingly, the genes covered by these neocentromeres maintained wild-type expression levels. In contrast to cen9∆ mutants, cen10Δ mutant strains exhibited growth defects and were aneuploid for chromosome 10. At an elevated growth temperature (37°C), the cen10Δ chromosome was found to have undergone fusion with another native chromosome in some isolates and this fusion restored wild-type growth. Following chromosomal fusion, the neocentromere was inactivated, and the native centromere of the fused chromosome served as the active centromere. The neocentromere formation and chromosomal fusion events observed in this study in C. deuterogattii may be similar to events that triggered genomic changes within the Cryptococcus/Kwoniella species complex and may contribute to speciation throughout the eukaryotic domain.

Data availability

ChIP and whole-genome sequencing reads and de novo genome assemblies were deposited under NCBI BioProject Accession ID: PRJNA511460.

The following data sets were generated
The following previously published data sets were used

Article and author information

Author details

  1. Klaas Schotanus

    Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, United States
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-0974-2882
  2. Joseph Heitman

    Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, United States
    For correspondence
    heitm001@duke.edu
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0001-6369-5995

Funding

NIH (AI050113-15)

  • Joseph Heitman

NIH (AI039115-22)

  • Joseph Heitman

CIFAR (Fungal Kingdom: Threats and Opportunities)

  • Joseph Heitman

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Reviewing Editor

  1. Wolf-Dietrich Heyer, University of California, Davis, United States

Publication history

  1. Received: February 14, 2020
  2. Accepted: April 16, 2020
  3. Accepted Manuscript published: April 20, 2020 (version 1)
  4. Version of Record published: April 28, 2020 (version 2)

Copyright

© 2020, Schotanus & Heitman

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.

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