Roig’s Lab

Lab Members

Ignasi Roig, PI
Montserrat Garcia Caldés
Ana Martínez Marchal
Andros Maldonado Linares
Yan Huang
Berta Cava
Eva Borreguero

Track record of the group

During my postdoc in the laboratory of Dr. S. Keeney (Howard Hughes Medical Institute and Memorial Sloan-Kettering Cancer Center, USA), I focused my research on the study of proteins involved in the regulation of meiotic recombination in mammals. First, I studied the role of one of the central DNA Damage Response (DDR) kinases, ATM, in meiotic prophase. Our study reported that ATM regulates homologous recombination and its outcomes during mammalian meiosis (Barchi and Roig et al., PLoS Genetics, 2008). In addition, I found and analyzed the function of the mouse homolog of PCH2, which regulates meiotic prophase progression in yeast. This study shows that the mammalian PCH2-homolog, TRIP13, has no apparent checkpoint function but is required to tie meiotic recombination progression with the development of higher order chromosomal structures (Roig et al., PLoS Genetics 2010). Also during my postdoc, I was involved in identifying the roles of two DDR proteins, p53 and ARF, in meiosis (Lu et al Science 2008 and Churchman et al. PLoS Genetics, 2011). These investigations revealed the tight connection between the DDR machinery and the control of meiotic prophase progression in mammals.

In 2009, I joined the Department of Cell Biology, Physiology and Immunology of the Universitat Autònoma de Barcelona as a lecturer, where I started my research group focused on understanding the mechanisms that regulate the progression of meiotic prophase in mammals. As a PI, I have obtained three Ministry of Economy and Competitiveness grants since 2009, (BFU2010-18965, BFU2013-43965-P and BFU2016-80370-P) and an award from the Association of Alumni of the UAB (Aposta 2011- 03). Our research has allowed us to identify that the DDR signaling pathway mediated by the MRE11 complex, ATM, CHK2, p53 and TAp63 controls the progression of spermatocytes with unrepaired DNA damage during meiotic prophase in mammals (Pacheco et al., PLoS Genetics 2015; Marcet-Ortega et al., PLoS Genetics 2017). At present, we are analyzing how this recombination-dependent checkpoint, regulated by CHK2, controls the fertile life-spam of mammalian females and its implication for human fertility. On the other hand, we have discovered the function of another major DDR kinase, ATR, in the meiotic recombination. In mouse, like in other model organisms, ATR favors homologous recombination, homologous chromosome synapsis, and synaptonemal complex formation during meiotic prophase (Pacheco et al, under review).Finally, we have uncovered that ATR function is critical for follicular cell development. This finding is very relevant for cancer patients going through chemotherapy with ATR inhibitors in order to predict its side effect on woman fertility after the treatment.

Altogether, our investigations focus on the interconnections between meiotic recombination, chromosome structure and cell cycle progression and how these processes are coordinated. We are currently expanding our knowledge of TRIP13 function in mammals and identifying other proteins involved in these processes in mammals.

Most relevant publications

  1. ATR Is Required To Complete Meiotic Recombination In Mice. Pacheco S, Maldonado-Linares A, Marcet-Ortega M, Rojas C, Martinez-Marchal A, Fuentes-Lazaro J, Lange J, Jasin M, Keeney S, Fernandez-Capetillo O, Garcia-Caldes M, Roig I. Under Review (bioRxiv 133744; doi:
  2. p53 and TAp63 participate in the recombination-dependent pachytene arrest in mouse spermatocytes. Marcet-Ortega M, Pacheco S, Martínez-Marchal A, Castillo H, Flores E, Jasin M, Keeney S, Roig I. PLoS Genet. 2017 Jun 15;13(6):e1006845. doi: 10.1371/journal.pgen.1006845.
  3. CEP63 deficiency promotes p53-dependent microcephaly and reveals a role for the centrosome in meiotic recombination. Marjanović M, Sánchez-Huertas C, Terré B, Gómez R, Scheel JF, Pacheco S, Knobel PA, Martínez-Marchal A, Aivio S, Palenzuela L, Wolfrum U, McKinnon PJ, Suja JA, Roig I, Costanzo V, Lüders J, Stracker TH. Nat Commun. 2015 Jul 9;6:7676. doi: 10.1038/ncomms8676.
  4. The ATM signaling cascade promotes recombination-dependent pachytene arrest in mouse spermatocytes. Pacheco S, Marcet-Ortega M, Lange J, Jasin M, Keeney S, Roig I. PLoS Genet. 2015 Mar 13;11(3):e1005017. doi: 10.1371/journal.pgen.1005017.
  5. Strong artificial selection in domestic mammals did not result in an increased recombination rate. Muñoz-Fuentes V, Marcet-Ortega M, Alkorta-Aranburu G, Linde Forsberg C, Morrell JM, Manzano-Piedras E, Söderberg A, Daniel K, Villalba A, Toth A, Di Rienzo A, Roig I, Vilà C. Mol Biol Evol. 2015 Feb;32(2):510-23. doi: 10.1093/molbev/msu322.
  6. The ATM signaling network in development and disease. Stracker TH, Roig I, Knobel PA, Marjanović M. Front Genet. 2013 Mar 25;4:37. doi: 10.3389/fgene.2013.00037.
  7. Presence of an extra chromosome alters meiotic double-stranded break repair dynamics and MLH1 foci distribution in human oocytes. Robles P, Roig I, Garcia R, Brieño-Enríquez M, Martin M, Cabero L, Toran N, Garcia Caldés M. Chromosoma. 2013 Mar;122(1-2):93-102. doi: 10.1007/s00412-012-0394-5. Epub 2013 Jan 4.
  8. Homeostatic control of recombination is implemented progressively in mouse meiosis. Cole F, Kauppi L, Lange J, Roig I, Wang R, Keeney S, Jasin M. Nat Cell Biol. 2012 Mar 4;14(4):424-30. doi: 10.1038/ncb2451.


Aim of the research work

The main objective of my research team is to deeply investigate the mechanisms that promote proper recombination and synapsis and control meiotic progression to understand the impact they have in fertility. Ultimately, by better understanding these processes we will be able to detect the mechanisms that originate important social problems like aneuploidy or infertility.

Specifically, we are focusing on two aspects that arise from our previous investigations. The first is the study of TRIP13 function during meiotic prophase. Our unpublished results showing TRIP13 is present at the telomeric regions of meiòtic chromosomes in the mouse are unexpected since it has not been reported for any other TRIP13 homolog. We are analyzing its possible functions in these chromosome regions as well as investigate the TRIP13-interacting partners responsible for this function. Also, since our previous studies revealed that TRIP13 regulates transcription of unsynapsed axes and silencing of unsynapsed chromosomes has been postulated to be the cause of the arrest resulting from synapsis failure, we are studying if TRIP13 deficiency rescues the arrest occurring in oocytes defective for homologous chromosome synapsis.

Lastly, our RNA sequencing from 14 days postpartum mouse testis reported the presence of multiple transcripts that did not map any annotated genes.  After an accurate in silico analysis, we have obtained a list of 104 putative novel genes. Thus, we are investigating the function of some of these putative novel genes in meiotic prophase progression using molecular biology, cell biology and genetic tools.

Research identification links

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