Identification of a Secondary Promoter within the Human B Cell Receptor Component Gene hCD79b

Yoo, Eung Jae; Cooke, Nancy E.; Liebhaber, Stephen A.

doi:10.1074/jbc.m113.461988

Cited by 4 publications

(7 citation statements)

References 46 publications

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“…Thus, to further test HSI-autonomy, we introduced a 1.6-kb interstitial deletion within the −8.0CD79b transgene that removed the hCD79b promoter along with a secondary promoter located within the first intron (− 8.0CD79bΔ1.6 ; Figure 1B ). The removal of these hCD79b promoters eliminates hCD79b transcription in B cells, but not in pituitary ( 25 ). Remarkably, each of 11 genetically distinct − 8.0CD79bΔ1.6 transgenic lines expressed appreciable levels of hCD79b mRNA in the pituitary.…”

Section: Resultsmentioning

confidence: 99%

“…The arrows indicate the distance between the HSI core and the center of the most proximal TSS cluster. hGH BAC , 123 kb unmodified human transgenic mouse line (two copies) ( 26 ); CDΔ0.7/hGH BAC , 0.7 kb deletion of 0.5 kb promoter region and exon 1 from hGH BAC (14 copies) ( 25 ); CDΔ1.6/hGH BAC , 1.6 kb deletion of 0.5 kb promoter through exon 2 from the hGH BAC (three copies) ( 23 ); −8.0CD79bΔ1.6 , 1.6 kb deletion of hCD79b promoter through exon 2 from the −8.0CD79b (6 copies); λΔCD/hGH BAC , 3.8 kb λ gene segment replacing hCD79b from hGH BAC (five copies) ( 23 ).…”

Section: Resultsmentioning

confidence: 99%

“…Each band signal was scanned and quantified using Typhoon FLA9500 Phosphorimager (GE Healthcare) and the normalized ratio was used to establish the transgene copy number. The transgenic lines hGH BAC, λΔCD/hGH BAC, CDΔ0.7/hGH BAC, CDΔ1.6/hGH BAC and − 8.0CD79b have been described previously ( 23 , 25 , 26 ).…”

Section: Methodsmentioning

confidence: 99%

“…Deletion of these determinants ablates hCD79b expression in B cells but has no impact on transcription across hCD79b in the pituitary ( 22 ). In a reciprocal manner, transcription of hCD79b in the pituitary is uniquely dependent on HSI function ( 22 , 23 ); targeted inactivation of HSI ablates hCD79b transcription in the pituitary but has no impact on hCD79b transcription in B cells ( 25 ). Importantly, the direct blockade of transcription across hCD79b in the pituitary represses hGH-N expression without altering HSI formation ( 19 ).…”

Section: Introductionmentioning

confidence: 99%

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Autonomous actions of the human growth hormone long-range enhancer

Yoo

Brown

Tsai

et al. 2015

Nucleic Acids Research

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The human growth hormone (hGH) gene is controlled by a long-range enhancer, HSI, located 14.5 kb 5′ to the hGH promoter. HSI establishes a domain of noncoding transcription that is ‘looped’ to the hGH promoter as an essential step in initiating hGH gene expression. Thus, defining how HSI generates its domain of noncoding transcription is central to understanding its long-range function. Here, we demonstrate that activation of noncoding transcription reflects an HSI-autonomous activity fully independent of interactions with linked gene promoters and occurring in spatial and temporal synchrony with initiation of GH expression in the embryonic pituitary. HSI establishes its noncoding transcription start sites (TSS) over a defined distance from its core determinants and in a manner independent of local primary sequences. The interval between HSI and it TSS co-maps with a domain of disordered and/or highly mobile nucleosomes specific to the pituitary locus. Thus, a localized chromatin reconfiguration by HSI and consequent establishment of an adjacent domain of noncoding transcription constitute initiating events in long-range enhancer function within the hGH locus.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Autonomous actions of the human growth hormone long-range enhancer

Yoo

Brown

Tsai

et al. 2015

Nucleic Acids Research

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“…Alternative promoters may exist in intergenic or intragenic regions [ 30 , 31 ]. Intragenic promoters have been described for transcription of tRNA and other non-coding (nc) RNAs [ 32 , 33 ] as well as protein-coding RNAs [ 31 , 34 – 38 ]. Recently, it has been reported that intragenic enhancers may act as alternative promoters transcribing multiple exonic poly(A) + RNA (meRNA) from host gene, although the function of meRNA remains unclear [ 39 ].…”

Section: Introductionmentioning

confidence: 99%

An unusual intragenic promoter ofPIWIL2contributes to aberrant activation of oncogenicPL2L60

Liu

et al. 2017

Oncotarget

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PIWIL2-like (PL2L) protein 60 (PL2L60), a product of aberrantly activated PIWIL2 gene, is widely expressed in various types of tumors and may promote tumorigenesis. However, the mechanisms underlying the activation of expression of PL2L60 remain unknown. In this study, an intragenic promoter responsible for the activation of PL2L60 within the human PIWIL2 gene has been identified, cloned and characterized. The promoter of PL2L60 is located in the intron 10 of the host gene PIWIL2. Bioinformatic and mutagenic analysis reveals that this intragenic promoter within the sequence of 50 nucleotides contains two closely arranged cis-acting elements specific for the hepatic leukemia factor (HLF) in the positive strand and signal transducer and activator of transcription 3 (STAT3) in the negative strand. Chromatin immunoprecipitation analysis demonstrates that both the HLF and polymerase II (Pol II), a hallmark of active promoters, directly bind to the sequence, although STAT3 does not. Knockdown of HLF and STAT3 alone or both by RNA interference significantly reduced both promoter activity and the PL2L60 protein expression, although there is no additive effect. The expression of PL2L60 proteins was enhanced when host gene Piwil2 was genetically disrupted in a murine cell model. Taken together, we have identified a PL2L60-specific intragenic promoter in the host gene of PIWIL2, which is interdependently activated by HLF and STAT3 through steric interaction. This activation is dependent on cellular milieu rather than the integrity of host gene PIWIL2, highlighting a novel, important mechanism for a cancer-causing gene to be activated during tumorigenesis.

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Exploring 3D chromatin contacts in gene regulation: The evolution of approaches for the identification of functional enhancer-promoter interaction

Zhang

et al. 2020

Computational and Structural Biotechnology Journal

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Identification of a Secondary Promoter within the Human B Cell Receptor Component Gene hCD79b

Cited by 4 publications

References 46 publications

Autonomous actions of the human growth hormone long-range enhancer

Autonomous actions of the human growth hormone long-range enhancer

An unusual intragenic promoter ofPIWIL2contributes to aberrant activation of oncogenicPL2L60

Exploring 3D chromatin contacts in gene regulation: The evolution of approaches for the identification of functional enhancer-promoter interaction

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