Monday, 04 July 2022
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UCELL CYCLE AND DEVELOPMENT UNIT

Connections between cell cycle regulators and developmental programs in simple eukaryotic organismses

 

 

  How growth and cell cycle progression are coordinately regulated during development in eukaryotic organisms is an active area of research. Extensive studies have led to a thorough understanding of the core mechanisms that drive the eukaryotic cell cycle. It has also become increasingly clear that these core mechanisms are modulated during development. Moreover, cell cycle regulators can in turn impart cell fate during development. The main idea we are trying to address is to assume that cell cycle regulators could have in eukaryotic cells new roles dedicated to determine developmental decisions. To proof the concept, we are using two distinct models of simple eukaryotic organisms: the phytopathogenic fungus Ustilago maydis and the nematode Caenorhabditis elegans.

 

The fungus U. maydis is perfectly suited to analyze the relationships between cell cycle, morphogenesis and pathogenicity. In this model system the activation of the virulence program involves the mating of a pair of compatible haploid budding cells to produce an infectious dikaryotic hypha. This process implies strong morphological changes (bud to hypha transition) as well as genetic changes (haploid to dikaryotic transition), advocating for an accurate control of the cell cycle and morphogenesis during these transitions. Our starting hypothesis is that the induction of the infective filament in U. maydis, the first step in the pathogenic process, relies on a dual process that involves by one side a specific cell cycle arrest and in other side the specific activation of a hyperpolarization growth. We believe that the impairment of any of these processes will have as an outcome the inhibition of the virulence. Our approaches involve three main objectives: 1) To study the mechanisms responsible of cell cycle arrest during infective filament formation. 2) To study how polar growth is regulated during the induction of the infective filament. 3) To study how the signal emanating from the transcriptional virulence program is transmitted to the cell cycle and morphogenetic regulators.

 

The second model system we are using is C. elegans, which offers a powerful model system to study cell division control during animal development. C. elegans have a transparent body and develop from the one-cell zygote to adult stage through a nearly invariant pattern of divisions. Thus, the division of all somatic cells can be followed within the developing animals and the exact times of cell division are known. In combination with efficient genetics, this allows for a sensitive identification of cell cycle mutants and quantitative analysis of cell-division defects at a resolution that exceeds the possibilities in other animal models. We are focused into the analysis of the connections between cell cycle regulation and chromatin regulators, since both the commitment and the maintenance of the distinct cell fates involve both cell cycle adjustment as well as formation of new chromatin landscapes.

   

RELEVANT PUBLICATIONS (2010-2021)

1. de la Torre, A., M. Jurca, K. Hofmann, L. Schmitz, K. Heimel, J. Kämper, and J. Pérez-Martín. Robust Cre recombinase activity in the biotrophic smut fungus Ustilago maydis enables efficient gene deletion to construct conditional null mutants in planta. Genetics en prensa (doi: 10.1093/genetics/iyab152.). 2021.

 

2. de la Torre, A., S. Castanheira and J. Pérez-Martín. Incompatibility between proliferation and plant invasion is mediated by a regulator of appressorium formation in the corn smut fungus Ustilago maydis. Proc. Natl. Acad. Sci. USA 117, 30599-30609. 2020.

 

3. Bardetti, P., S. Castanheira, O. Valerius, G. H. Braus, and J. Pérez-Martín. Cytoplasmic retention and degradation of a mitotic inducer enable plant infection by a pathogenic fungus. eLIFE 20, e48943. 2019.

 

4. Pérez-Martín, J., P. Bardetti, S. Castanheira, A. de la Torre and Tenorio-Gomez M. Virulence-specific cell cycle and morphogenesis connections in pathogenic fungi. Semin. Cell Dev. Biol. 57, 93-99. 2016.

 

5. de Sena-Tomás, C., E.Y. Yu, A. Calzada, W.K. Holloman, N.F. Lue and J. Pérez-Martín. Fungal Ku prevents permanent cell cycle arrest by suppressing DNA damage signaling at telomeres. Nucleic Acid Res. 43, 2138-2151. 2015.

 

6. Castanheira, S., N. Mielnichuk and J. Pérez-Martín. Programmed cell cycle arrest is required for infection of corn plants by the fungus Ustilago maydis. Development 141, 4817-4826. 2014.

 

7. de Sena-Tomás, C., M. Navarro-Gonzalez, U. Kues and J. Pérez-Martín. A DNA damage checkpoint pathway coordinates the division of dikaryotic cells in the ink cap mushroom Coprinopsis cinerea. Genetics 195, 47-57. 2013.

 

8. Sartorel, E. and J. Pérez-Martín. The distinct interaction between cell cycle regulation and the widely conserved Morphogenesis-Related (MOR) pathway in the fungus Ustilago maydis determines morphology. J. Cell Sci. 125, 4597-4608. 2012.

 

9. de Sena-Tomás, C., A. Fernandez-Alvarez, W. K. Holloman, and J. Pérez-Martín. DNA-damage-response-signaling cascade regulates proliferation of the phytopathogenic fungus Ustilago maydis in planta. Plant Cell 23, 1654-1665. 2011.

 

10. Carbó, N. and J. Pérez-Martín. Activation of the Cell Wall Integrity pathway promotes escape from G2 in the fungus Ustilago maydis. PLoS Genetics 6, 1001009. 2010.

 



 

 

  

 

 

 
 

  Principal Investigator:

 José Pérez

 
 
Currículum Vitae

Publicaciones

 Teléfono: 963391760

Email: jperezibv.csic.es

 
     
 
  • Pérez Martín, José
  • Alós Hernández, Álvaro
  • Puerta Martos, David