Gene transcriptions/X core promoter element 1

< Gene transcriptions
The image shows a group of people gathered to promote a computer game. Credit: - EMR -.

The core promoter element X core promoter element 1 (XCPE1) directs activator-, mediator-, protein-dependent but TFIID-independent RNA polymerase II transcription from TATA box-less promoters.[1]

This promoter element appears to be exclusively human such as the group in the image at the right.

Consensus sequences

"[T]he X gene core promoter element 1 ... is located between nucleotides -8 and +2 relative to the transcriptional start site (+1) and has a consensus sequence of G/A/T-G/C-G-T/C-G-G-G/A-A-G/C+1-A/C."[1]

Gene expressions

Although it is harder to regulate the transcription of genes with multiple transcription start sites, "variations in the expression of a constitutive gene would be minimized by the use of multiple start sites."[2]

Human genes

"XCPE1 is ... found in the core promoter regions of about 1% of human genes, particularly in poorly characterized TATA-less genes."[1]

Gene transcriptions

"From a teleological standpoint, this arrangement [of focused promoters] is consistent with the notion that it would be easier to regulate the transcription of a gene with a single transcription start site than one with multiple start sites."[2]

Focused promoters

"In focused transcription, there is either a single major transcription start site or several start sites within a narrow region of several nucleotides. Focused transcription is the predominant mode of transcription in simpler organisms."[2]

"Focused transcription initiation occurs in all organisms, and appears to be the predominant or exclusive mode of transcription in simpler organisms."[2]

"In vertebrates, focused transcription tends to be associated with regulated promoters".[2]

"The analysis of focused core promoters has led to the discovery of sequence motifs such as the TATA box, BREu (upstream TFIIBrecognition element), Inr (initiator), MTE (motif ten element), DPE (downstream promoter element), DCE (downstream core element), and XCPE1 (Xcore promoter element 1) [...]."[2]

Dispersed promoters

"In dispersed transcription, there are several weak transcription start sites over a broad region of about 50 to 100 nucleotides. Dispersed transcription is the most common mode of transcription in vertebrates. For instance, dispersed transcription is observed in about two-thirds of human genes."[2]

In vertebrates, "dispersed transcription is typically observed in constitutive promoters in CpG islands."[2]

Core promoter

"Focused transcription typically initiates within the Inr, and the A nucleotide in the Inr consensus is usually designed as the “+ 1” position, whether or not transcription actually initiates at that particular nucleotide. This convention is useful because other core promoter motifs, such as the MTE and DPE, function with the Inr in a manner that exhibits a strict spacing dependence with the Inr consensus sequence (and hence, the A + 1 nucleotide) rather than the actual transcription start site (Burke and Kadonaga, 1997, Kutach and Kadonaga, 2000 and Lim et al., 2004)."[2]

"NC2 (negative cofactor 2; also known as Dr1-Drap1) [...] was identified as repressor of TATA-dependent transcription [...]."[2]

"Several core promoter elements have been previously identified in eukaryotes, but those cannot account for transcription from most RNA polymerase II-transcribed genes."[1]

Research

Hypothesis:

  1. XCPE1 does not participate in the transcription of A1BG.

Control groups

This is an image of a Lewis rat. Credit: Charles River Laboratories.

The findings demonstrate a statistically systematic change from the status quo or the control group.

“In the design of experiments, treatments [or special properties or characteristics] are applied to [or observed in] experimental units in the treatment group(s).[3] In comparative experiments, members of the complementary group, the control group, receive either no treatment or a standard treatment.[4]"[5]

Proof of concept

Def. a “short and/or incomplete realization of a certain method or idea to demonstrate its feasibility"[6] is called a proof of concept.

Def. evidence that demonstrates that a concept is possible is called proof of concept.

The proof-of-concept structure consists of

  1. background,
  2. procedures,
  3. findings, and
  4. interpretation.[7]

See also

References

  1. 1 2 3 4 Yumiko Tokusumi, Ying Ma, Xianzhou Song, Raymond H. Jacobson, and Shinako Takada (March 2007). "The New Core Promoter Element XCPE1 (X Core Promoter Element 1) Directs Activator-, Mediator-, and TATA-Binding Protein-Dependent but TFIID-Independent RNA Polymerase II Transcription from TATA-Less Promoters". Molecular and Cellular Biology 27 (5): 1844-58. doi:10.1128/MCB.01363-06. PMID 17210644. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1820453/. Retrieved 2013-02-09.
  2. 1 2 3 4 5 6 7 8 9 10 Tamar Juven-Gershon and James T. Kadonaga (15 March 2010). "Regulation of gene expression via the core promoter and the basal transcriptional machinery". Developmental Biology 339 (2): 225-9. doi:10.1016/j.ydbio.2009.08.009. http://www.sciencedirect.com/science/article/pii/S0012160609011166. Retrieved 2016-01-16.
  3. ↑ Klaus Hinkelmann, Oscar Kempthorne (2008). Design and Analysis of Experiments, Volume I: Introduction to Experimental Design (2nd ed.). Wiley. ISBN 978-0-471-72756-9. http://books.google.com/?id=T3wWj2kVYZgC&printsec=frontcover.
  4. ↑ R. A. Bailey (2008). Design of comparative experiments. Cambridge University Press. ISBN 978-0-521-68357-9. http://www.cambridge.org/uk/catalogue/catalogue.asp?isbn=9780521683579.
  5. ↑ "Treatment and control groups, In: Wikipedia". San Francisco, California: Wikimedia Foundation, Inc. May 18, 2012. Retrieved 2012-05-31.
  6. ↑ "proof of concept, In: Wiktionary". San Francisco, California: Wikimedia Foundation, Inc. November 10, 2012. Retrieved 2013-01-13.
  7. ↑ Ginger Lehrman and Ian B Hogue, Sarah Palmer, Cheryl Jennings, Celsa A Spina, Ann Wiegand, Alan L Landay, Robert W Coombs, Douglas D Richman, John W Mellors, John M Coffin, Ronald J Bosch, David M Margolis (August 13, 2005). "Depletion of latent HIV-1 infection in vivo: a proof-of-concept study". Lancet 366 (9485): 549-55. doi:10.1016/S0140-6736(05)67098-5. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1894952/. Retrieved 2012-05-09.

Further reading

External links

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