Selenoprotein N is dynamically expressed during mouse development and detected early in muscle precursors

doi:10.1186/1471-213X-9-46

BMC Developmental Biology
Volume 9

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Castets P
Maugenre S
Gartioux C
Rederstorff M
Krol A
Lescure A
Tajbakhsh S
Allamand V
Guicheney P

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Castets P
Maugenre S
Gartioux C
Rederstorff M
Krol A
Lescure A
Tajbakhsh S
Allamand V
Guicheney P
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Research article

Selenoprotein N is dynamically expressed during mouse development and detected early in muscle precursors

Perrine Castets¹^,2^,6 , Svetlana Maugenre¹^,2^,6 , Corine Gartioux¹^,2^,7 , Mathieu Rederstorff³^,8 , Alain Krol³ , Alain Lescure³ , Shahragim Tajbakhsh⁴ , Valérie Allamand¹^,2^,7 and Pascale Guicheney¹^,2^,5^,6

¹Inserm, U582, F-75013 Paris, France

²UPMC Univ Paris 06, UMR_S582, Institut de Myologie, IFR14, F-75013 Paris, France

³Architecture et Réactivité de l'ARN, Université de Strasbourg, CNRS, IBMC, F-67084 Strasbourg, France

⁴CNRS, URA 2578, Institut Pasteur, F-75015 Paris, France

⁵AP-HP, Groupe Hospitalier Pitié-Salpêtrière, Service de Biochimie Métabolique, F-75013 Paris, France

⁶Inserm, U956, UPMC Univ Paris 06, UMR_S956, F-75013 Paris, France

⁷Inserm, U974, Institut de Myologie, CNRS UMR7215, UPMC Univ Paris 06, UMR_S974, IFR14, F-75013 Paris, France

⁸Innsbruck Medical University, Biocenter, Section for Genomics and RNomics, A-6020 Innsbruck, Austria

author email corresponding author email

BMC Developmental Biology 2009, 9:46doi:10.1186/1471-213X-9-46


Published:	22 August 2009

Abstract

Background

In humans, mutations in the SEPN1 gene, encoding selenoprotein N (SelN), are involved in early onset recessive neuromuscular disorders, referred to as SEPN1-related-myopathies. The mechanisms behind these pathologies are poorly understood since the function of SelN remains elusive. However, previous results obtained in humans and more recently in zebrafish pointed to a potential role for SelN during embryogenesis. Using qRT-PCR, Western blot and whole mount in situ hybridization, we characterized in detail the spatio-temporal expression pattern of the murine Sepn1 gene during development, focusing particularly on skeletal muscles.

Results

In whole embryos, Sepn1 transcripts were detected as early as E5.5, with expression levels peaking at E12.5, and then strongly decreasing until birth. In isolated tissues, only mild transcriptional variations were observed during development, whereas a striking reduction of the protein expression was detected during the perinatal period. Furthermore, we demonstrated that Sepn1 is expressed early in somites and restricted to the myotome, the sub-ectodermal mesenchyme and the dorsal root ganglia at mid-gestation stages. Interestingly, Sepn1 deficiency did not alter somitogenesis in embryos, suggesting that SelN is dispensable for these processes in mouse.

Conclusion

We characterized for the first time the expression pattern of Sepn1 during mammalian embryogenesis and we demonstrated that its differential expression is most likely dependent on major post-transcriptional regulations. Overall, our data strongly suggest a potential role for selenoprotein N from mid-gestation stages to the perinatal period. Interestingly, its specific expression pattern could be related to the current hypothesis that selenoprotein N may regulate the activity of the ryanodine receptors.