Sertoli cell-specific ablation of miR-17-92 cluster significantly alters whole testis transcriptome without apparent phenotypic effects
Metadatos
Mostrar el registro completo del ítemAutor
Hurtado, Alicia; Real, Francisca M.; Palomino Morales, Rogelio Jesús; Carmona López, Francisco David; Burgos Poyatos, Miguel; Jiménez Medina, Rafael; Barrionuevo Jiménez, Francisco JavierEditorial
Public Library of Science (PLOS)
Fecha
2018-05-24Referencia bibliográfica
Hurtado A, Real FM, Palomino R, Carmona FD, Burgos M, Jiménez R, et al. (2018) Sertoli cell-specific ablation of miR-17-92 cluster significantly alters whole testis transcriptome without apparent phenotypic effects. PLoS ONE 13 (5). [http://hdl.handle.net/10481/54820]
Patrocinador
This work was supported by grants from the Andalusian Government, Junta de Andalucía, BIO-109 to R. Jiménez and P11-CVI-7291 to M. Burgos and grants from the Spanish Ministry of Science and Innovation (CGL2011-23368 and CGL2015-67108-P) to R. Jiménez and F.J. Barrionuevo. The authors would like to thank the Spanish Ministry of Science and Innovation for the 'Ramón y Cajal' fellowship granted to F.D. Carmona (RYC-2014-16458) and the 'FPU' PhD fellowship granted to A. Hurtado.Resumen
MicroRNAs are frequently organized into polycistronic clusters whose transcription is controlled
by a single promoter. The miR-17-92 cluster is expressed in most embryonic and
postnatal organs. It is a potent oncogene associated to several types of cancer and it is
involved in several important developmental processes. In the testis, expression of the miR-
17-92 cluster in the germ cells is necessary to maintain normal spermatogenesis. This cluster
is also expressed in Sertoli cells (the somatic cells of the seminiferous tubules), which
require miRNAs for correct cell development and survival. To study the possible role of miR-
17-92 in Sertoli cell development and function and, in order to overcome the postnatal lethality
of miR-17-92-/ mice, we conditionally deleted it in embryonic Sertoli cells shortly after the
sex determination stage using an Amh-Cre allele. Mutant mice developed apparently normal
testes and were fertile, but their testis transcriptomes contained hundreds of moderately
deregulated genes, indicating that testis homeostasis is tightly controlled in mammals and
that miR-17-92 expression in Sertoli cells contribute to maintain normal gene expression
levels, but is unnecessary for testis development and function. Our results show that significant
deregulation of hundreds of genes might have no functional consequences.