Tasks performed
- Administrative Coordinator CRESCO - Centre for Embryology and Healthy Development
Background
Publications
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Zhao, Xu; Hendriks, Ivo A; Gras, Stephanie Le; Ye, Tao; Alonso, Lucia Ramos & P, Aurélie Nguéa
[Show all 13 contributors for this article]
(2022).
Waves of sumoylation support transcription dynamics during adipocyte differentiation.
Nucleic Acids Research (NAR).
ISSN 0305-1048.
50(3),
p. 1351–1369.
doi:
10.1093/nar/gkac027.
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Abstract Tight control of gene expression networks required for adipose tissue formation and plasticity is essential for adaptation to energy needs and environmental cues. However, the mechanisms that orchestrate the global and dramatic transcriptional changes leading to adipocyte differentiation remain to be fully unraveled. We investigated the regulation of nascent transcription by the sumoylation pathway during adipocyte differentiation using SLAMseq and ChIPseq. We discovered that the sumoylation pathway has a dual function in differentiation; it supports the initial downregulation of pre-adipocyte-specific genes, while it promotes the establishment of the mature adipocyte transcriptional program. By characterizing endogenous sumoylome dynamics in differentiating adipocytes by mass spectrometry, we found that sumoylation of specific transcription factors like PPARγ/RXR and their co-factors are associated with the transcription of adipogenic genes. Finally, using RXR as a model, we found that sumoylation may regulate adipogenic transcription by supporting the chromatin occurrence of transcription factors. Our data demonstrate that the sumoylation pathway supports the rewiring of transcriptional networks required for formation of functional adipocytes. This study also provides the scientists in the field of cellular differentiation and development with an in-depth resource of the dynamics of the SUMO-chromatin landscape, SUMO-regulated transcription and endogenous sumoylation sites during adipocyte differentiation.
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Born, Erwin Van den; Vågbø, Cathrine Broberg; Songe-Møller, Lene; Leihne, VIbeke; Lien, Guro Flor & Leszczynska, G
[Show all 11 contributors for this article]
(2011).
ALKBH8-mediated formation of a novel diastereomeric pair of wobble nucleosides in mammalian tRNA.
Nature Communications.
2.
doi:
10.1038/ncomms1173.
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Mammals have nine different homologues (ALKBH1–9) of the Escherichia coli DNA repair demethylase AlkB. ALKBH2 is a genuine DNA repair enzyme, but the in vivo function of the other ALKBH proteins has remained elusive. It was recently shown that ALKBH8 contains an additional transfer RNA (tRNA) methyltransferase domain, which generates the wobble nucleoside 5-methoxycarbonylmethyluridine (mcm5U) from its precursor 5-carboxymethyluridine (cm5U). In this study, we report that (R)- and (S)-5-methoxycarbonylhydroxymethyluridine (mchm5U), hydroxylated forms of mcm5U, are present in mammalian , and , respectively, representing the first example of a diastereomeric pair of modified RNA nucleosides. Through in vitro and in vivo studies, we show that both diastereomers of mchm5U are generated from mcm5U, and that the AlkB domain of ALKBH8 specifically hydroxylates mcm5U into (S)-mchm5U in . These findings expand the function of the ALKBH oxygenases beyond nucleic acid repair and increase the current knowledge on mammalian wobble uridine modifications and their biogenesis.
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Nordstrand, Line Mari; Svärd, Jessica; Larsen, Elisabeth; Nilsen, Anja; Ougland, Rune & Furu, Kari
[Show all 11 contributors for this article]
(2010).
Mice Lacking Alkbh1 Display Sex-Ratio Distortion and Unilateral Eye Defects.
PLOS ONE.
5(11).
doi:
10.1371/journal.pone.0013827.
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Background Eschericia coli AlkB is a 2-oxoglutarate- and iron-dependent dioxygenase that reverses alkylated DNA damage by oxidative demethylation. Mouse AlkB homolog 1 (Alkbh1) is one of eight members of the newly discovered family of mammalian dioxygenases. Methods and Findings In the present study we show non-Mendelian inheritance of the Alkbh1 targeted allele in mice. Both Alkbh1−/− and heterozygous Alkbh1+/− offspring are born at a greatly reduced frequency. Additionally, the sex-ratio is considerably skewed against female offspring, with one female born for every three to four males. Most mechanisms that cause segregation distortion, act in the male gametes and affect male fertility. The skewing of the sexes appears to be of paternal origin, and might be set in the pachythene stage of meiosis during spermatogenesis, in which Alkbh1 is upregulated more than 10-fold. In testes, apoptotic spermatids were revealed in 5–10% of the tubules in Alkbh1−/− adults. The deficiency of Alkbh1 also causes misexpression of Bmp2, 4 and 7 at E11.5 during embryonic development. This is consistent with the incompletely penetrant phenotypes observed, particularly recurrent unilateral eye defects and craniofacial malformations. Conclusions Genetic and phenotypic assessment suggests that Alkbh1 mediates gene regulation in spermatogenesis, and that Alkbh1 is essential for normal sex-ratio distribution and embryonic development in mice. © 2010 Nordstrand et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Flato, B; Lien, Guro Flor; Smerdel-Ramoya, A & Vinje, O
(2008).
Juvenile psoriatic arthritis - Outcome and differentiation from other subtypes of juvenile idiopathic arthritis.
Arthritis and Rheumatism.
ISSN 0004-3591.
58,
p. S710–S711.
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Published
Sep. 20, 2023 12:15 PM
- Last modified
Oct. 22, 2025 7:33 PM
