| TAZ-TFM-2017-935 |
Regulación Epigenética del locus Cd9 por REX1
Guevara Rodríguez, Susana
Schoorlemmer, Jon (dir.) ; Climent Aroz, María (dir.)
Universidad de Zaragoza,
CIEN,
2017
Bioquímica y Biología Molecular y Celular department, Bioquímica y Biología Molecular area
Máster en Biología Molecular y Celular
Tipo de Trabajo Académico: Trabajo Fin de Master
Notas: The transcription factor REX1 controls the methylation levels of imprinted genes during early embryogenesis and participates in the silencing of endogenous retroviruses (ERVs). It has been found by ChiPseq that this factor targets the Cd9 gene which encodes a protein with the same name that participates in multiple biological activities. This relationship suggests that REX1 act as a transcriptional regulator of Cd9 by epigenetic mechanisms. In the present work, we studied whether REX1 is able to modulate the expression of CD9 locus. To this end, the percent methylation of Cd9 genomic sequences close to the ChiPseq peak and the levels of RNA expression of the Cd9 locus by qPCR were determined. We analyzed cells and tissue samples from mouse (ES, TS, placentas and embryos) wt and compared them with REX1 - / - and REX1 +/-. The results indicated that REX1 acts as a protector of methylation of the Cd9 locus and repressor of its expression. This effect seems to be unrelated because there is no negative correlation between the degree of methylation of the analysed locus in these tissues and the levels of Cd9 expression. It is possible that this region is not determinant for the control of its expression, or other regulatory mechanisms of transcription are acting.
Notas: The transcription factor REX1 controls the methylation levels of imprinted genes during early embryogenesis and participates in the silencing of endogenous retroviruses (ERVs). It has been found by ChiPseq that this factor targets the Cd9 gene which encodes a protein with the same name that participates in multiple biological activities. This relationship suggests that REX1 act as a transcriptional regulator of Cd9 by epigenetic mechanisms. In the present work, we studied whether REX1 is able to modulate the expression of CD9 locus. To this end, the percent methylation of Cd9 genomic sequences close to the ChiPseq peak and the levels of RNA expression of the Cd9 locus by qPCR were determined. We analyzed cells and tissue samples from mouse (ES, TS, placentas and embryos) wt and compared them with REX1 - / - and REX1 +/-. The results indicated that REX1 acts as a protector of methylation of the Cd9 locus and repressor of its expression. This effect seems to be unrelated because there is no negative correlation between the degree of methylation of the analysed locus in these tissues and the levels of Cd9 expression. It is possible that this region is not determinant for the control of its expression, or other regulatory mechanisms of transcription are acting.
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