4.8 Article

Unlinking an lncRNA from Its Associated cis Element

期刊

MOLECULAR CELL
卷 62, 期 1, 页码 104-110

出版社

CELL PRESS
DOI: 10.1016/j.molcel.2016.02.029

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资金

  1. ASH Scholar Award
  2. University of Pennsylvania Measey Fellowship Award
  3. NIDDK T32 training grant
  4. NIDDK [K08 1K08DK102533-01A1, R01 DK092318, R56 DK065806]
  5. NHLBI [RO1HL119479]
  6. Wellcome Trust [098931/Z/12/Z, 106130/Z/14/Z]
  7. Medical Research Council [4050189188]
  8. MRC [MR/N00969X/1, MC_UU_12009/15] Funding Source: UKRI
  9. Medical Research Council [MC_UU_12009/15, MR/N00969X/1] Funding Source: researchfish
  10. Wellcome Trust [098931/Z/12/Z] Funding Source: Wellcome Trust

向作者/读者索取更多资源

Long non-coding (lnc) RNAs can regulate gene expression and protein functions. However, the proportion of lncRNAs with biological activities among the thousands expressed in mammalian cells is controversial. We studied Lockd (lncRNA downstream of Cdkn1b), a 434-nt polyadenylated lncRNA originating 4 kb 3' to the Cdkn1b gene. Deletion of the 25-kb Lockd locus reduced Cdkn1b transcription by approximately 70% in an erythroid cell line. In contrast, homozygous insertion of a polyadenylation cassette 80 bp downstream of the Lockd transcription start site reduced the entire lncRNA transcript level by >90% with no effect on Cdkn1b transcription. The Lockd promoter contains a DNase-hypersensitive site, binds numerous transcription factors, and physically associates with the Cdkn1b promoter in chromosomal conformation capture studies. Therefore, the Lockd gene positively regulates Cdkn1b transcription through an enhancer-like cis element, whereas the lncRNA itself is dispensable, which may be the case for other lncRNAs.

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