TY - JOUR
T1 - Transcriptional activation of mouse retrotransposons in vivo
T2 - Specific expression in steroidogenic cells in response to trophic hormones
AU - Schiff, Rachel
AU - Itin, Ahuva
AU - Keshet, Eli
PY - 1991
Y1 - 1991
N2 - Transcription of cellular retrotransposons is induced by a variety of physiological stimuli. We have used in situ hybridization analysis to determine the cell types in which mouse retrotransposons are transcriptionally activated in vivo under physiological conditions. Here, we report that VL30 retrotransposons are specifically expressed in steroidogenic cells within all four endocrine tissues engaged in synthesis of steroid hormones in response to the respective pituitary-derived trophic hormones. These tissues include ovarian steroidogenic theca cells and lutein cells of the corpus luteum, testosterone-producing Leydig cells of the testis, steroidogenic cells confined to the zona reticularis of the adrenal cortex, and progesterone-producing cells of the placenta. In the course of preovulatory follicular development and maturation, the profile of cells expressing the retrotransposon shifted in parallel to the changing profiles of the leutinizing hormone (LH)-induced steroidogenic output of the respective cells. Expression of VL30 in both male and female gonads was shown to be greatly stimulated by external administration of gonadotropins. In vitro studies using a LH-responsive Leydig cell line have confirmed that expression of the resident retrotransposons is gonadotropin dependent. Run-off transcription assays have indicated that activation is at the transcriptional level. To allow molecular access to gonadatropin-activated transcription units, the long terminal repeat (LTR) regulatory domains were cloned from VL30 cDNAs of LH-induced ovaries. Through the use of reporter gene constructs and transfection experiments it was shown that expression of these elements in steroidogenic cells is LH dependent. Furthermore, cAMP, a known mediator of trophic hormone responses, could replace the hormone for inducibility. Transfection studies have also shown that the retrotransposon LTRs may function as hormone-activated enhancers conferring a LH-dependent phenotype on a surrogate transcription unit. These studies have thus demonstrated that the transcriptional activation of resident retrotransposons in vivo is a dynamic process that can be modulated by gonadotropins and have the potential of imposing this phenotype on adjacent cellular genes.
AB - Transcription of cellular retrotransposons is induced by a variety of physiological stimuli. We have used in situ hybridization analysis to determine the cell types in which mouse retrotransposons are transcriptionally activated in vivo under physiological conditions. Here, we report that VL30 retrotransposons are specifically expressed in steroidogenic cells within all four endocrine tissues engaged in synthesis of steroid hormones in response to the respective pituitary-derived trophic hormones. These tissues include ovarian steroidogenic theca cells and lutein cells of the corpus luteum, testosterone-producing Leydig cells of the testis, steroidogenic cells confined to the zona reticularis of the adrenal cortex, and progesterone-producing cells of the placenta. In the course of preovulatory follicular development and maturation, the profile of cells expressing the retrotransposon shifted in parallel to the changing profiles of the leutinizing hormone (LH)-induced steroidogenic output of the respective cells. Expression of VL30 in both male and female gonads was shown to be greatly stimulated by external administration of gonadotropins. In vitro studies using a LH-responsive Leydig cell line have confirmed that expression of the resident retrotransposons is gonadotropin dependent. Run-off transcription assays have indicated that activation is at the transcriptional level. To allow molecular access to gonadatropin-activated transcription units, the long terminal repeat (LTR) regulatory domains were cloned from VL30 cDNAs of LH-induced ovaries. Through the use of reporter gene constructs and transfection experiments it was shown that expression of these elements in steroidogenic cells is LH dependent. Furthermore, cAMP, a known mediator of trophic hormone responses, could replace the hormone for inducibility. Transfection studies have also shown that the retrotransposon LTRs may function as hormone-activated enhancers conferring a LH-dependent phenotype on a surrogate transcription unit. These studies have thus demonstrated that the transcriptional activation of resident retrotransposons in vivo is a dynamic process that can be modulated by gonadotropins and have the potential of imposing this phenotype on adjacent cellular genes.
KW - Gonadotropins
KW - In situ hybridization
KW - Retrotransposons
KW - Steroidogenesis
KW - VL30
UR - http://www.scopus.com/inward/record.url?scp=0025877254&partnerID=8YFLogxK
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C2 - 1849106
AN - SCOPUS:0025877254
SN - 0890-9369
VL - 5
SP - 521
EP - 532
JO - Genes and Development
JF - Genes and Development
IS - 4
ER -