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 Integration of Growth and Cell Size via the TOR Pathway and the Dot6 Transcription Factor in Candida albicans

Genetics ◽  
2018 ◽  
Vol 211 (2) ◽  
pp. 637-650 ◽  
Author(s):  
Julien Chaillot ◽  
Faiza Tebbji ◽  
Jaideep Mallick ◽  
Adnane Sellam
Keyword(s):  
Transcription Factor ◽  
Candida Albicans ◽  
Cell Size ◽  
Tor Pathway

scholarly journals Roles of Candida albicans Sfl1 in Hyphal Development

2007 ◽  
Vol 6 (11) ◽  
pp. 2112-2121 ◽  
Author(s):  
Yandong Li ◽  
Chang Su ◽  
Xuming Mao ◽  
Fang Cao ◽  
Jiangye Chen
Keyword(s):  
Candida Albicans ◽  
Growth Conditions ◽  
Filamentous Growth ◽  
Negative Regulator ◽  
Specific Gene ◽  
Environmental Cues ◽  
Dimorphic Fungi ◽  
Hyphal Development ◽  
Negative Factor ◽  
Functional Homolog

ABSTRACT The ability to switch between different morphological forms is an important feature of Candida albicans and is relevant to its pathogenesis. Many conserved positive and negative transcription factors are involved in morphogenetic regulation of the two dimorphic fungi Candida albicans and Saccharomyces cerevisiae. In S. cerevisiae, the transcriptional repressor Sfl1 and the activator Flo8 function antagonistically in invasive and filamentous growth. We have previously reported that Candida albicans Flo8 is a transcription factor essential for hyphal development and virulence in C. albicans. To determine whether a similar negative factor exists in C. albicans, we identified Candida albicans Sfl1 as a functional homolog of the S. cerevisiae sfl1 mutant. Sfl1 is a negative regulator of hyphal development in C. albicans. Deletion of C. albicans SFL1 enhanced filamentous growth and hypha-specific gene expression in several media and at several growth temperatures. Overexpression of the SFL1 led to a significant reduction of filament formation. Both deletion and overexpression of the SFL1 attenuated virulence of C. albicans in a mouse model. Deleting FLO8 in an sfl1/sfl1 mutant completely blocked hyphal development in various growth conditions examined, suggesting that C. albicans Sfl1 may act as a negative regulator of filamentous growth by antagonizing Flo8 functions. We suggest that, similar to the case for S. cerevisiae, a combination of dual control by activation and repression of Flo8 and Sfl1 may contribute to the fine regulatory network in C. albicans morphogenesis responding to different environmental cues.

scholarly journals Surface-to-volume scaling and aspect ratio preservation in rod-shaped bacteria

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Nikola Ojkic ◽  
Diana Serbanescu ◽  
Shiladitya Banerjee
Keyword(s):  
Aspect Ratio ◽  
Cell Size ◽  
Bacterial Cell ◽  
Environmental Changes ◽  
Morphological Changes ◽  
Size Control ◽  
Growth Conditions ◽  
Quantitative Agreement ◽  
Quantitative Model ◽  
Bacterial Cells

Rod-shaped bacterial cells can readily adapt their lengths and widths in response to environmental changes. While many recent studies have focused on the mechanisms underlying bacterial cell size control, it remains largely unknown how the coupling between cell length and width results in robust control of rod-like bacterial shapes. In this study we uncover a conserved surface-to-volume scaling relation in Escherichia coli and other rod-shaped bacteria, resulting from the preservation of cell aspect ratio. To explain the mechanistic origin of aspect-ratio control, we propose a quantitative model for the coupling between bacterial cell elongation and the accumulation of an essential division protein, FtsZ. This model reveals a mechanism for why bacterial aspect ratio is independent of cell size and growth conditions, and predicts cell morphological changes in response to nutrient perturbations, antibiotics, MreB or FtsZ depletion, in quantitative agreement with experimental data.

scholarly journals A new class of cyclin dependent kinase in Chlamydomonas is required for coupling cell size to cell division

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Yubing Li ◽  
Dianyi Liu ◽  
Cristina López-Paz ◽  
Bradley JSC Olson ◽  
James G Umen
Keyword(s):  
Cell Division ◽  
Cell Size ◽  
Mother Cell ◽  
Size Control ◽  
Mitotic Division ◽  
General Mechanism ◽  
Cell Cycle Regulators ◽  
Proliferating Cells ◽  
Multiple Fission ◽  
Division Number

Proliferating cells actively control their size by mechanisms that are poorly understood. The unicellular green alga Chlamydomonas reinhardtii divides by multiple fission, wherein a ‘counting’ mechanism couples mother cell-size to cell division number allowing production of uniform-sized daughters. We identified a sizer protein, CDKG1, that acts through the retinoblastoma (RB) tumor suppressor pathway as a D-cyclin-dependent RB kinase to regulate mitotic counting. Loss of CDKG1 leads to fewer mitotic divisions and large daughters, while mis-expression of CDKG1 causes supernumerous mitotic divisions and small daughters. The concentration of nuclear-localized CDKG1 in pre-mitotic cells is set by mother cell size, and its progressive dilution and degradation with each round of cell division may provide a link between mother cell-size and mitotic division number. Cell-size-dependent accumulation of limiting cell cycle regulators such as CDKG1 is a potentially general mechanism for size control.

scholarly journals The size-wise nucleus: nuclear volume control in eukaryotes

2007 ◽  
Vol 179 (4) ◽  
pp. 583-584 ◽  
Author(s):  
Michael D. Huber ◽  
Larry Gerace
Keyword(s):  
Fission Yeast ◽  
Cell Size ◽  
Size Control ◽  
Growth Conditions ◽  
Nuclear Size ◽  
Yeast Cells ◽  
Volume Control ◽  
Wide Range ◽  
The Relationship

Eukaryotic cells have an “awareness” of their volume and organellar volumes, and maintain a nuclear size that is proportional to the total cell size. New studies in budding and fission yeast have examined the relationship between cell and nuclear volumes. It was found that the size of the nucleus remains proportional to cell size in a wide range of genetic backgrounds and growth conditions that alter cell volume and DNA content. Moreover, in multinucleated fission yeast cells, Neumann and Nurse (see p. 593 of this issue) found that the sizes of individual nuclei are controlled by the relative amount of cytoplasm surrounding each nucleus. These results highlight a role of the cytoplasm in nuclear size control.

scholarly journals SETD2 negatively regulates cell size through its catalytic activity and SRI domain

2021 ◽  
Author(s):  
Thom M Molenaar ◽  
Eliza Mari Kwesi-Maliepaard ◽  
Joana Silva ◽  
Muddassir Malik ◽  
William J Faller ◽  
...  
Keyword(s):  
Catalytic Activity ◽  
Rna Polymerase Ii ◽  
Cell Size ◽  
Cell Function ◽  
Size Control ◽  
Cell Types ◽  
Negative Regulator ◽  
Cellular Functions ◽  
Global Protein Synthesis

Cell size varies between cell types but is tightly regulated by cell-intrinsic and extrinsic mechanisms. Cell-size control is important for cell function and changes in cell size are frequently observed in cancer cells. Here we uncover a non-canonical role of SETD2 in regulating cell size. SETD2 is a lysine methyltransferase and a tumor suppressor protein involved in transcription regulation, RNA processing and DNA repair. At the molecular level, SETD2 is best known for associating with RNA polymerase II through its Set2-Rbp1 interacting (SRI) domain and methylating histone H3 on lysine 36 (H3K36) during transcription. Although most of the cellular functions of SETD2 have been linked to this activity, several non-histone substrates of SETD2 have recently been identified, some of which have been linked to novel functions of SETD2 beyond chromatin regulation. Using multiple, independent perturbation strategies we identify SETD2 as a negative regulator of global protein synthesis rates and cell size. We provide evidence that this function is dependent on the catalytic activity of SETD2 but independent of H3K36 methylation. Paradoxically, ectopic overexpression of a decoy SRI domain also increased cell size, suggesting that the relevant substrate is engaged by SETD2 via its SRI domain. These data add a central role of SETD2 in regulating cellular physiology and warrant further studies on separating the different functions of SETD2 in cancer development.

scholarly journals Direct and indirect regulation of Pom1 cell size pathway by the protein phosphatase 2C Ptc1

2020 ◽  
Author(s):  
Veneta Gerganova ◽  
Payal Bhatia ◽  
Sophie G Martin
Keyword(s):  
Cell Size ◽  
Size Control ◽  
Negative Regulator ◽  
Yeast Cells ◽  
Concentration Gradients ◽  
Important Pathway ◽  
Low Glucose ◽  
Constant Cell ◽  
Cell Size Control

AbstractThe fission yeast cells Schizosaccharomyces pombe divide at constant cell size regulated by environmental stimuli. An important pathway of cell size control involves the membrane-associated DYRK-family kinase Pom1, which forms decreasing concentration gradients from cell poles and inhibits mitotic inducers at mid-cell. Here, we identify the phosphatase 2C Ptc1 as negative regulator of Pom1. Ptc1 localizes to cell poles in a manner dependent on polarity and cell-wall integrity factors. We show that Ptc1 directly binds Pom1 and can dephosphorylate it in vitro but modulates Pom1 localization indirectly upon growth in low glucose conditions by influencing microtubule stability. Thus, Ptc1 phosphatase plays both direct and indirect roles in the Pom1 cell size control pathway.

scholarly journals Initiation of chromosome replication controls both division and replication cycles in E. coli through a double-adder mechanism

2019 ◽  
Author(s):  
Guillaume Witz ◽  
Erik van Nimwegen ◽  
Thomas Julou
Keyword(s):  
Cell Cycle ◽  
Cell Size ◽  
Cell Cycle Control ◽  
Size Control ◽  
Time Lapse ◽  
Growth Conditions ◽  
Replication Initiation ◽  
Stochastic Simulations ◽  
E Coli ◽  
Wide Range

AbstractLiving cells proliferate by completing and coordinating two essential cycles, a division cycle that controls cell size, and a DNA replication cycle that controls the number of chromosomal copies in the cell. Despite lacking dedicated cell cycle control regulators such as cyclins in eukaryotes, bacteria such as E. coli manage to tightly coordinate those two cycles across a wide range of growth conditions, including situations where multiple nested rounds of replication progress simultaneously. Various cell cycle models have been proposed to explain this feat, but it has been impossible to validate them so far due to a lack of experimental tools for systematically testing their different predictions. Recently new insights have been gained on the division cycle through the study of the structure of fluctuations in growth, size, and division in individual cells. In particular, it was found that cell size appears to be controlled by an adder mechanism, i.e. the added volume between divisions is held approximately constant and fluctuates independently of growth rate and cell size at birth. However, how replication initiation is regulated and coupled to cell size control remains unclear, mainly due to scarcity of experimental measurements on replication initiation at the single-cell level. Here, we used time-lapse microscopy in combination with microfluidics to directly measure growth, division and replication in thousands of single E. coli cells growing in both slow and fast growth conditions. In order to compare different phenomenological models of the cell cycle, we introduce a statistical framework which assess their ability to capture the correlation structure observed in the experimental data. Using this in combination with stochastic simulations, our data indicate that, instead of thinking of the cell cycle as running from birth to division, the cell cycle is controlled by two adder mechanisms starting at the initiation of replication: the added volume since the last initiation event controls the timing of both the next division event and the next replication initiation event. Interestingly the double-adder mechanism identified in this study has recently been found to explain the more complex cell cycle of mycobacteria, suggesting shared control strategies across species.

scholarly journals Revisiting the role of yeast Sfp1 in ribosome biogenesis and cell size control: a chemostat study

Microbiology ◽  
2008 ◽  
Vol 154 (1) ◽  
pp. 337-346 ◽  
Author(s):  
Chiara Cipollina ◽  
Joost van den Brink ◽  
Pascale Daran-Lapujade ◽  
Jack T. Pronk ◽  
Marina Vai ◽  
...  
Keyword(s):  
Cell Size ◽  
Ribosome Biogenesis ◽  
Size Control ◽  
Cell Size Control

scholarly journals Universal surface-to-volume scaling and aspect ratio homeostasis in rod-shaped bacteria

2019 ◽  
Author(s):  
Nikola Ojkic ◽  
Diana Serbanescu ◽  
Shiladitya Banerjee
Keyword(s):  
Aspect Ratio ◽  
Cell Size ◽  
Bacterial Cell ◽  
Environmental Changes ◽  
Morphological Changes ◽  
Size Control ◽  
Growth Conditions ◽  
Quantitative Agreement ◽  
Quantitative Model ◽  
Bacterial Cells

AbstractRod-shaped bacterial cells can readily adapt their lengths and widths in response to environmental changes. While many recent studies have focused on the mechanisms underlying bacterial cell size control, it remains largely unknown how the coupling between cell length and width results in robust control of rod-like bacterial shapes. In this study we uncover a universal surface-to-volume scaling relation in Escherichia coli and other rod-shaped bacteria, resulting from the preservation of cell aspect ratio. To explain the mechanistic origin of aspect-ratio control, we propose a quantitative model for the coupling between bacterial cell elongation and the accumulation of an essential division protein, FtsZ. This model reveals a mechanism for why bacterial aspect ratio is independent of cell size and growth conditions, and predicts cell morphological changes in response to nutrient perturbations, antibiotics, MreB or FtsZ depletion, in quantitative agreement with experimental data.

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