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Gene Review:

Kcnq1ot1 - KCNQ1 overlapping transcript 1

Mus musculus

Synonyms: Kvlqt1-as, Lit1, Tssc8

Thakur, N. et al., Pandey, R.R. et al., Lewis, A. et al., Mancini-Dinardo, D. et al., Yatsuki, H. et al., et al.

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High impact information on Kcnq1ot1

The KvDMR, which maps within intron 10 of Kcnq1, contains the promoter for a paternally expressed, noncoding, antisense transcript, Kcnq1ot1 [1].
We show that the lack of a full-length Kcnq1ot1 transcript on the paternal chromosome leads to the expression of genes that are normally paternally repressed [1].
Elongation of the Kcnq1ot1 transcript is required for genomic imprinting of neighboring genes [1].
To elucidate whether the Kcnq1ot1 RNA plays a role in the bidirectional silencing activity of the Kcnq1 ICR, we have characterized factor binding sites by genomic footprinting and tested the functional consequence of various deletions of these binding sites in an episome-based system [2].
Furthermore, interruption of Kcnq1ot1 RNA production by the insertion of a polyadenylation sequence downstream of the promoter also caused a loss of both silencing activity and methylation spreading [2].

Biological context of Kcnq1ot1

The conserved region includes the recently identified KCNQ1OT1/Kcnq1ot1 antisense transcripts, flanked by a strikingly conserved cluster of LINE/Line elements and a CpG island which we show to carry a maternal germline methylation imprint [3].
In this investigation, using genomic footprinting, we have identified three NF-Y transcription factor binding sites appearing in a methylation-sensitive manner in the Kcnq1ot1 promoter [4].
Parallel to the loss of antisense transcription, the loss of silencing of the flanking reporter genes was observed, suggesting that NF-Y-mediated Kcnq1ot1 transcription is critical in the bidirectional silencing process of the Kcnq1 ICR [4].
Maternal repression of Kcnq1ot1 is controlled by DNA methylation originating in the oocyte [5].

Anatomical context of Kcnq1ot1

Placentally imprinted genes that are distal to Kcnq1ot1, by contrast, are not imprinted in blastocysts, ES or TS cells [5].
By contrast, genes that are only imprinted in the placenta, while regulated by the same non-coding RNA transcript Kcnq1ot1, undergo epigenetic inactivation during differentiation of the trophoblast lineage [5].

Other interactions of Kcnq1ot1

Three genes, Lit1 (Kvlqt1-AS), Mtr1 and Tssc4, were identified and characterized [6].
Domain regulation of imprinting cluster in Kip2/Lit1 subdomain on mouse chromosome 7F4/F5: large-scale DNA methylation analysis reveals that DMR-Lit1 is a putative imprinting control region [7].

References

Elongation of the Kcnq1ot1 transcript is required for genomic imprinting of neighboring genes. Mancini-Dinardo, D., Steele, S.J., Levorse, J.M., Ingram, R.S., Tilghman, S.M. Genes Dev. (2006) [Pubmed]
An antisense RNA regulates the bidirectional silencing property of the Kcnq1 imprinting control region. Thakur, N., Tiwari, V.K., Thomassin, H., Pandey, R.R., Kanduri, M., Göndör, A., Grange, T., Ohlsson, R., Kanduri, C. Mol. Cell. Biol. (2004) [Pubmed]
Sequence and functional comparison in the Beckwith-Wiedemann region: implications for a novel imprinting centre and extended imprinting. Engemann, S., Strödicke, M., Paulsen, M., Franck, O., Reinhardt, R., Lane, N., Reik, W., Walter, J. Hum. Mol. Genet. (2000) [Pubmed]
NF-Y regulates the antisense promoter, bidirectional silencing, and differential epigenetic marks of the Kcnq1 imprinting control region. Pandey, R.R., Ceribelli, M., Singh, P.B., Ericsson, J., Mantovani, R., Kanduri, C. J. Biol. Chem. (2004) [Pubmed]
Epigenetic dynamics of the Kcnq1 imprinted domain in the early embryo. Lewis, A., Green, K., Dawson, C., Redrup, L., Huynh, K.D., Lee, J.T., Hemberger, M., Reik, W. Development (2006) [Pubmed]
Sequence-based structural features between Kvlqt1 and Tapa1 on mouse chromosome 7F4/F5 corresponding to the Beckwith-Wiedemann syndrome region on human 11p15.5: long-stretches of unusually well conserved intronic sequences of kvlqt1 between mouse and human. Yatsuki, H., Watanabe, H., Hattori, M., Joh, K., Soejima, H., Komoda, H., Xin, Z., Zhu, X., Higashimoto, K., Nishimura, M., Kuratomi, S., Sasaki, H., Sakaki, Y., Mukai, T. DNA Res. (2000) [Pubmed]
Domain regulation of imprinting cluster in Kip2/Lit1 subdomain on mouse chromosome 7F4/F5: large-scale DNA methylation analysis reveals that DMR-Lit1 is a putative imprinting control region. Yatsuki, H., Joh, K., Higashimoto, K., Soejima, H., Arai, Y., Wang, Y., Hatada, I., Obata, Y., Morisaki, H., Zhang, Z., Nakagawachi, T., Satoh, Y., Mukai, T. Genome Res. (2004) [Pubmed]

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