scholarly journals Genome-wide screen for haploinsufficient cell size genes in the opportunistic yeast Candida albicans

2016 ◽  
Author(s):  
Julien Chaillot ◽  
Michael A Cook ◽  
Jacques Corbeil ◽  
Adnane Sellam
Keyword(s):  
Candida Albicans ◽  
Cell Division ◽  
Cell Size ◽  
Pathogenic Fungi ◽  
Eukaryotic Cell ◽  
Restriction Point ◽  
Genome Wide ◽  
Comprehensive Survey ◽  
Size Threshold ◽  
Commitment To Cell Division

ABSTRACTOne of the most critical but still poorly understood aspects of eukaryotic cell proliferation is the basis for commitment to cell division in late G1 phase called Start in yeast and the Restriction Point in metazoans. In all species, a critical cell size threshold coordinates cell growth with cell division and thereby establishes a homeostatic cell size. While a comprehensive survey of cell size genetic determinism has been performed in the saprophytic yeasts Saccharomyces cerevisiae and Schizosaccharomyces pombe, very little is known in pathogenic fungi. As a number of critical Start regulators are haploinsufficient for cell size, we applied a quantitative analysis of the size phenome, using elutriation-barcode sequencing methodology, to 5,639 barcoded heterozygous deletion strains in the opportunistic yeast Candida albicans. Our screen identified conserved known regulators and biological processes required to maintain size homeostasis in addition to novel C. albicans specific size genes, and provided a conceptual framework for future mechanistic studies. Interestingly, some of the size genes identified were required for fungal pathogenicity suggesting that cell size homeostasis may be elemental to C. albicans fitness or virulence inside the host.

scholarly journals Genome-Wide Screen for Haploinsufficient Cell Size Genes in the Opportunistic Yeast Candida albicans

2016 ◽  
Vol 7 (2) ◽  
pp. 355-360 ◽  
Author(s):  
Julien Chaillot ◽  
Michael A. Cook ◽  
Jacques Corbeil ◽  
Adnane Sellam
Keyword(s):  
Candida Albicans ◽  
Cell Size ◽  
Genome Wide

scholarly journals Transcriptional Networks Controlling the Cell Cycle

2013 ◽  
Vol 3 (1) ◽  
pp. 75-90 ◽  
Author(s):  
Martin Bonke ◽  
Mikko Turunen ◽  
Maria Sokolova ◽  
Anna Vähärautio ◽  
Teemu Kivioja ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Cell Size ◽  
Transcriptional Networks ◽  
Protein Homeostasis ◽  
Transcriptional Program ◽  
Regulatory Systems ◽  
Genome Wide ◽  
A Genome ◽  
Division Process

Abstract In this work, we map the transcriptional targets of 107 previously identified Drosophila genes whose loss caused the strongest cell-cycle phenotypes in a genome-wide RNA interference screen and mine the resulting data computationally. Besides confirming existing knowledge, the analysis revealed several regulatory systems, among which were two highly-specific and interconnected feedback circuits, one between the ribosome and the proteasome that controls overall protein homeostasis, and the other between the ribosome and Myc/Max that regulates the protein synthesis capacity of cells. We also identified a set of genes that alter the timing of mitosis without affecting gene expression, indicating that the cyclic transcriptional program that produces the components required for cell division can be partially uncoupled from the cell division process itself. These genes all have a function in a pathway that regulates the phosphorylation state of Cdk1. We provide evidence showing that this pathway is involved in regulation of cell size, indicating that a Cdk1-regulated cell size checkpoint exists in metazoans.

scholarly journals Dot6 is a major regulator of cell size and a transcriptional activator of ribosome biogenesis in the opportunistic yeast Candida albicans

2018 ◽  
Author(s):  
Julien Chaillot ◽  
Jaideep Malick ◽  
Adnane Sellam
Keyword(s):  
Candida Albicans ◽  
Cell Size ◽  
Ribosome Biogenesis ◽  
Size Control ◽  
Transcriptional Activator ◽  
Growth Conditions ◽  
Mitotic Division ◽  
Negative Regulator ◽  
Restriction Point ◽  
Tor Pathway

AbstractIn most species, size homeostasis appears to be exerted in late G1 phase as cells commit to division, called Start in yeast and the Restriction Point in metazoans. This size threshold couples cell growth to division and thereby establishes long-term size homeostasis. Our former investigations have shown that hundreds of genes markedly altered cell size under homeostatic growth conditions in the opportunistic yeast Candida albicans, but surprisingly only few of these overlapped with size control genes in the budding yeast Saccharomyces cerevisiae. Here, we investigated one of the divergent potent size regulators in C. albicans, the Myb-like HTH transcription factor Dot6. Our data demonstrated that Dot6 is a negative regulator of Start and also acts as a transcriptional activator of ribosome biogenesis (Ribi) genes. Genetic epistasis uncovered that Dot6 interacted with the master transcriptional regulator of the G1 machinery, SBF complex, but not with the Ribi and cell size regulators Sch9, Sfp1 and p38/Hog1. Dot6 was required for carbon-source modulation of cell size and it is regulated at the level of nuclear localization by TOR pathway. Our findings support a model where Dot6 acts as a hub that integrate directly growth cues via the TOR pathway to control the commitment to mitotic division at G1.

scholarly journals Cysteine-Rich Hydrophobin Gene Family: Genome Wide Analysis, Phylogeny and Transcript Profiling in Cordyceps militaris

2021 ◽  
Vol 22 (2) ◽  
pp. 643
Author(s):  
Xiao Li ◽  
Fen Wang ◽  
Yanyan Xu ◽  
Guijun Liu ◽  
Caihong Dong
Keyword(s):  
Life Cycle ◽  
Pathogenic Fungi ◽  
Class Ii ◽  
Cordyceps Militaris ◽  
Transcript Profiling ◽  
Saprotrophic Fungi ◽  
Genome Wide Analysis ◽  
Genome Wide ◽  
Encoding Genes

Hydrophobins are a family of small secreted proteins found exclusively in fungi, and they play various roles in the life cycle. In the present study, genome wide analysis and transcript profiling of the hydrophobin family in Cordyceps militaris, a well-known edible and medicinal mushroom, were studied. The distribution of hydrophobins in ascomycetes with different lifestyles showed that pathogenic fungi had significantly more hydrophobins than saprotrophic fungi, and class II members accounted for the majority. Phylogenetic analysis of hydrophobin proteins from the species of Cordyceps s.l. indicated that there was more variability among the class II members than class I. Only a few hydrophobin-encoding genes evolved by duplication in Cordyceps s.l., which was inconsistent with the important role of gene duplication in basidiomycetes. Different transcript patterns of four hydrophobin-encoding genes during the life cycle indicated the possible different functions for each. The transcripts of Cmhyd2, 3 and 4 can respond to light and were related with the photoreceptors. CmQHYD, with four hydrophobin II domains, was first found in C. militaris, and multi-domain hydrophobins were only distributed in the species of Cordycipitaceae and Clavicipitaceae. These results could be helpful for further function research of hydrophobins and could provide valuable information for the evolution of hydrophobins.

scholarly journals Genome-wide mapping of DNA double-strand breaks from eukaryotic cell cultures using Break-seq

2021 ◽  
Vol 2 (2) ◽  
pp. 100554
Author(s):  
Ishita Joshi ◽  
Jenna DeRycke ◽  
Megan Palmowski ◽  
Robert LeSuer ◽  
Wenyi Feng
Keyword(s):  
Cell Cultures ◽  
Eukaryotic Cell ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Strand Breaks ◽  
Genome Wide

scholarly journals Replicative Aging in Pathogenic Fungi

2020 ◽  
Vol 7 (1) ◽  
pp. 6
Author(s):  
Somanon Bhattacharya ◽  
Tejas Bouklas ◽  
Bettina C. Fries
Keyword(s):  
Cell Division ◽  
Candida Glabrata ◽  
Asymmetric Cell Division ◽  
Pathogenic Fungi ◽  
Yeast Cells ◽  
Candida Auris ◽  
Replicative Aging ◽  
Yeast Saccharomyces Cerevisiae ◽  
Phenotypic Variations ◽  
Systemic Infections

Candida albicans, Candida auris, Candida glabrata, and Cryptococcus neoformans are pathogenic yeasts which can cause systemic infections in immune-compromised as well as immune-competent individuals. These yeasts undergo replicative aging analogous to a process first described in the nonpathogenic yeast Saccharomyces cerevisiae. The hallmark of replicative aging is the asymmetric cell division of mother yeast cells that leads to the production of a phenotypically distinct daughter cell. Several techniques to study aging that have been pioneered in S. cerevisiae have been adapted to study aging in other pathogenic yeasts. The studies indicate that aging is relevant for virulence in pathogenic fungi. As the mother yeast cell progressively ages, every ensuing asymmetric cell division leads to striking phenotypic changes, which results in increased antifungal and antiphagocytic resistance. This review summarizes the various techniques that are used to study replicative aging in pathogenic fungi along with their limitations. Additionally, the review summarizes some key phenotypic variations that have been identified and are associated with changes in virulence or resistance and thus promote persistence of older cells.

scholarly journals Interdependent YpsA- and YfhS-Mediated Cell Division and Cell Size Phenotypes in Bacillus subtilis

mSphere ◽  
2020 ◽  
Vol 5 (4) ◽  
Author(s):  
Robert S. Brzozowski ◽  
Brooke R. Tomlinson ◽  
Michael D. Sacco ◽  
Judy J. Chen ◽  
Anika N. Ali ◽  
...  
Keyword(s):  
Bacillus Subtilis ◽  
Cell Division ◽  
Cell Size ◽  
Unknown Function ◽  
Suppressor Mutation ◽  
Gram Positive ◽  
Content Type ◽  
Suppressor Mutations ◽  
Extragenic Suppressor ◽  
Cell Division Inhibition

ABSTRACT Although many bacterial cell division factors have been uncovered over the years, evidence from recent studies points to the existence of yet-to-be-discovered factors involved in cell division regulation. Thus, it is important to identify factors and conditions that regulate cell division to obtain a better understanding of this fundamental biological process. We recently reported that in the Gram-positive organisms Bacillus subtilis and Staphylococcus aureus, increased production of YpsA resulted in cell division inhibition. In this study, we isolated spontaneous suppressor mutations to uncover critical residues of YpsA and the pathways through which YpsA may exert its function. Using this technique, we were able to isolate four unique intragenic suppressor mutations in ypsA (E55D, P79L, R111P, and G132E) that rendered the mutated YpsA nontoxic upon overproduction. We also isolated an extragenic suppressor mutation in yfhS, a gene that encodes a protein of unknown function. Subsequent analysis confirmed that cells lacking yfhS were unable to undergo filamentation in response to YpsA overproduction. We also serendipitously discovered that YfhS may play a role in cell size regulation. Finally, we provide evidence showing a mechanistic link between YpsA and YfhS. IMPORTANCE Bacillus subtilis is a rod-shaped Gram-positive model organism. The factors fundamental to the maintenance of cell shape and cell division are of major interest. We show that increased expression of ypsA results in cell division inhibition and impairment of colony formation on solid medium. Colonies that do arise possess compensatory suppressor mutations. We have isolated multiple intragenic (within ypsA) mutants and an extragenic suppressor mutant. Further analysis of the extragenic suppressor mutation led to a protein of unknown function, YfhS, which appears to play a role in regulating cell size. In addition to confirming that the cell division phenotype associated with YpsA is disrupted in a yfhS-null strain, we also discovered that the cell size phenotype of the yfhS knockout mutant is abolished in a strain that also lacks ypsA. This highlights a potential mechanistic link between these two proteins; however, the underlying molecular mechanism remains to be elucidated.

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