Absence of a spindle position checkpoint in the fungal pathogen Cryptococcus neoformans
- 1New York University
Abstract
To maintain genome stability, it is crucial that cells do not initiate cytokinesis until chromosomes have been properly segregated. In the model budding yeast Saccharomyces cerevisiae, a surveillance mechanism called the Spindle Position Checkpoint (SPoC) ensures this coordination by regulating the Mitotic Exit Network (MEN) to couple exit from mitosis and cytokinesis to spindle position. The MEN is conserved in Ascomycota where the orthologous pathway in the fission yeast Schizosaccharomyces pombe, the Septation Initiation Network (SIN), regulates cytokinesis in response to defects in spindle elongation. Here, we show that the MEN/SIN pathway is conserved in the basidiomycetous budding yeast and human pathogen, Cryptococcus neoformans, and controls cytokinesis. However, spindle position or elongation does not regulate pathway activation or cell cycle progression in C. neoformans. In essence, there appears to be no SPoC in this organism to delay cytokinesis upon defects in mitosis. We speculate that while increasing the risk of genome instability, the lack of a SPoC might facilitate C. neoformans's ability to change ploidy in the host.
Related
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BibTeX
@misc{wang2026absence,
title = {{Absence of a spindle position checkpoint in the fungal pathogen Cryptococcus neoformans}},
author = {T. K. Wang and J. Matthews and A. Strege and E. Wallace and X. Zhou},
howpublished = {bioRxiv},
year = {2026},
month = aug,
doi = {10.64898/2026.08.31.748335},
url = {https://www.biorxiv.org/content/10.64898/2026.08.31.748335v1},
note = {CC BY-NC-ND},
}
RIS
TY - UNPB
TI - Absence of a spindle position checkpoint in the fungal pathogen Cryptococcus neoformans
AU - T. K. Wang
AU - J. Matthews
AU - A. Strege
AU - E. Wallace
AU - X. Zhou
PY - 2026
DA - 2026/08/31
PB - bioRxiv
DO - 10.64898/2026.08.31.748335
UR - https://www.biorxiv.org/content/10.64898/2026.08.31.748335v1
AB - To maintain genome stability, it is crucial that cells do not initiate cytokinesis until chromosomes have been properly segregated. In the model budding yeast Saccharomyces cerevisiae, a surveillance mechanism called the Spindle Position Checkpoint (SPoC) ensures this coordination by regulating the Mitotic Exit Network (MEN) to couple exit from mitosis and cytokinesis to spindle position. The MEN is conserved in Ascomycota where the orthologous pathway in the fission yeast Schizosaccharomyces pombe, the Septation Initiation Network (SIN), regulates cytokinesis in response to defects in spindle elongation. Here, we show that the MEN/SIN pathway is conserved in the basidiomycetous budding yeast and human pathogen, Cryptococcus neoformans, and controls cytokinesis. However, spindle position or elongation does not regulate pathway activation or cell cycle progression in C. neoformans. In essence, there appears to be no SPoC in this organism to delay cytokinesis upon defects in mitosis. We speculate that while increasing the risk of genome instability, the lack of a SPoC might facilitate C. neoformans's ability to change ploidy in the host.
ER -