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Modeling human diseases in C. elegans

imatge Central Grup Recerca

Scientific Team

Researchers
Julian Ceron
Postdoctoral researchers
Montserrat Porta
Predoctoral researchers
Karinna denise Rubio, Xènia Serrat


Research lines

 

1- RNA PROCESSING AND DISEASE
Mechanisms of RNA processing are highly conserved from yeast to humans and necessary to
transfer DNA information to protein synthesis. Therefore, this process is essential for gene
expression programs and is frequently altered in human diseases. While most of the
information about RNA processing comes from biochemical and in vitro studies, we use the
multicellular organism C. elegans because of its powerful genetic and genomic tools to shed
light on steps of RNA metabolism that are impaired in diverse diseases.
2- CANCER
Most of the mechanisms that contribute to the onset and development of cancer are conserved
along evolution. In C. elegans we study why disruption of gene functions can contribute to
genome instability, cell death or uncontrolled cell divisions.
Interestingly, many of the chemotherapies and radiotherapies applied to humans also produce
an effect in worms. We are studying mechanisms that confer sensitivity and resistance to these
therapies against cancer.

1- RNA PROCESSING AND DISEASE

Mechanisms of RNA processing are highly conserved from yeast to humans and necessary to transfer DNA information to protein synthesis. Therefore, this process is essential for gene expression programs and is frequently altered in human diseases. While most of theinformation about RNA processing comes from biochemical and in vitro studies, we use the multicellular organism C. elegans because of its powerful genetic and genomic tools to shed light on steps of RNA metabolism that are impaired in diverse diseases.

 

2- CANCER

Most of the mechanisms that contribute to the onset and development of cancer are conservedalong evolution. In C. elegans we study why disruption of gene functions can contribute to genome instability, cell death or uncontrolled cell divisions. Interestingly, many of the chemotherapies and radiotherapies applied to humans also produce an effect in worms. We are studying mechanisms that confer sensitivity and resistance to these therapies against cancer.


Five most recent papers published:

 

  • Loss of the proteostasis factor AIRAPL causes myeloid transformation byderegulating IGF-1 signaling. Osorio FG, Soria-Valles C, Santiago-Fernández O, Bernal T,2,Mittelbrunn M, Colado E, Rodríguez F, Bonzon-Kulichenko E, Vázquez J, Porta-de-la-Riva M,Cerón J, Fueyo A Li J, Green AR1, Freije JM, López-Otín C. Nature Medicine. 2016Jan;22(1):91-6.3.2.2.
  • Functional Interplay of Two Paralogs Encoding SWI/SNF Chromatin-Remodeling Accessory Subunits During Caenorhabditis elegans Development. Ertl I, Porta-de-la-Riva M,Gómez-Orte E, Rubio K, Aristizábal-Corrales D, Cornes E, Fontrodona L, Osteikoetxea X,Ayuso C, Askjaer P, Cabello J, Cerón J*. Genetics. 2016 Jan 6. pii: genetics.115.183533.3.2.3. 
  • Cytoplasmic LSM-1 protein regulates stress responses through the insulin/IGF-1signaling pathway in Caenorhabditis elegans. Cornes E, Porta-De-La-Riva M, Aristizábal Corrales D, Brokate-Llanos AM, García-Rodríguez FJ, Ertl I, Díaz M, Fontrodona L, Reis K,Johnsen R, Baillie D, Muñoz MJ, Sarov M, Dupuy D, Cerón J*. RNA. 2015 Jul 6. doi: 10.12613.2.4. 
  • Modeling of autosomal-dominant retinitis pigmentosa in Caenorhabditis elegansuncovers a nexus between global impaired functioning of certain splicing factors and cell typespecificapoptosis. Rubio-Peña K, Fontrodona L, Aristizábal-Corrales D, Torres S, Cornes E,García-Rodríguez FJ, Serrat X, González-Knowles D, Foissac S, Porta-De-La-Riva M, CerónJ*. RNA. 2015 Dec;21(12):2119-31. doi: 10.1261/rna.053397.115.3.2.5. 
  • Co-option of the piRNA pathway for germline-specific alternative splicing of C. elegans TOR. Barberán-Soler S, Fontrodona L, Ribó A, Lamm AT, Iannone C, Cerón J, Lehner B,Valcárcel J. Cell Reports 2014 Sep 25;8(6):1609-16. doi: 10.1016/j.celrep.2014.08.016. Epub2014 Sep 15.3.3) 

Five most cited papers:

  • Jean-François Rual*; Julian Ceron*; John Koreth; Tong Hao; Anne-Sophie Nicot;Tomoko Hirozane Kishikawa; Jean Vandenhaute; Stuart H Orkin; David E Hill; Sander van denHeuvel; Marc Vidal. Toward improving Caenorhabditis elegans phenome mapping with anORFeome-based RNAi library. Genome Research. 14 - 10B, pp. 2162 - 2170. Citations: 371
  • Johnathan R Whetstine; Julian Ceron; Brendon Ladd; Pascale Dufourcq; Valerie Reinke;Yang Shi. Regulation of tissue-specific and extracellular matrix-related genes by a class Ihistone deacetylase.Molecular Cell. 18 - 4, pp. 483 - 573. 13/05/2005. Citations: 51
  • Julian Ceron; Jean-François Rual; Abha Chandra; Denis Dupuy; Marc Vidal; Sander vanden Heuvel. Large-scale RNAi screens identify novel genes that interact with the C. elegansretinoblastoma pathway as well as splicing-related components with synMuv B activity.BMCDevelopmental Biology. 7, pp. 30. 2007. Citations: 50
  • Frédérique Gay; Dominica Calvo; Miao-Chia Lo; Julian Ceron; Morris Maduro; RueylingLin; Yang Shi. Acetylation regulates subcellular localization of the Wnt signaling nucleareffector POP-1.Genes & Development. 17 - 6, pp. 717 - 739. 15/03/2003. Citations: 38
  • Montserrat Porta de-la-Riva; Laura Fontrodona; Alberto Villanueva; Julián Cerón*. BasicCaenorhabditis elegans methods: synchronization and observation.Journal of visualizedexperiments : JoVE. pp. e4019. 2012. Available at: .Citations:11

Agency: Instituto de Salud Carlos III

Title: C. elegans como modelo de enfermedades: uso de CRISPR/Cas9 parainvestigar respuestas a fármacos y patologías relacionadas con alteraciones enfactores de splicing.

IP: Julián Cerón Madrigal

N Participants: 4

Period: 1/01/2016 to 31/12/2018

Amount: 159.115€

Ref: PI15/00895

 

Agency: Instituto de Salud Carlos III

Title: Caenorhabditis elegans como modelo de estudio de genes implicados enenfermedades humanas: nuevos conceptos funcionales en la regulación de la expresióngénica.

IP: Julián Cerón Madrigal

N Participants: 5

Period: 01/01/2013 - 31/12/2015

Amount: 110.715 €

Ref: PI12/01554

 

Agency: Fundacio Marató TV3

Title: Functional roles of splicing factors in autosomal dominat Retinitis Pigmentosa(ad-RP): uncovering molecular mechanisms in Caenorhabditis elegans to explore noveltherapies

IP: Julián Cerón Madrigal

N Participants: 5

Period: 01/01/2011 - 31/12/2014

Amount: 182.000 €

 

Agency: AGAUR-CTP

Title: Implicacions del gen LSm1 en càncer i estudi del seu potencial com a dianaterapèutica.

IPs: Julián Cerón and Denis Dupuy

N Participants: 3

Period: 01/06/2013 - 31/10/2013

Amount: 8430 €

 

Agency: Instituto de Salud Carlos III

Title: Towards a functional map of splicing-related genes.

IP: Julián Cerón Madrigal

N Participants: 3

Period: 01/01/2010 - 31/12/2012

Amount: 98.000 €

 

Agency: International Reintegration Grant - Curie

Title: Modeling cancer in Caenorhabditis elegans-IRG-Curie.

IP: Julián Cerón Madrigal

N Participants: 1

Period: 01/11/2008 - 01/04/2012

Amount: 100.000 €

imatge personal
 

Group leader

Julian Ceron
Telephone  
+34 932607251
E-mail  
jceron@idibell.cat
 
© 2017 Institut d'Investigació Biomèdica de Bellvitge



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