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As human females have two [[X chromosome|X chromosomes]], this means they have the ability to produce twice as much X-linked gene product, this Dosage Compensation Mechanism is responsible for&nbsp;keeping levels of the X-linked gene product similar in both males and females. Therefore, such a mechanism only exists in females. Dosage compensation requires [[RNA polymerase|RNA polymerase]], [[Tsix transcript|Tsix transcript]] and [[Xist transcript|Xist transcript]] as well as the X chromosomes of developing embryonic cells. Note that each transcript is transcribed on one [[Chromosome|chromosome]] each. Xist acts as to ensure inactivation of X chromosome whereas Tsix ensures X chromosome remains active. Such activity is carried out from the [[X inactivation centre|X inactivation centre]]&nbsp;<ref>Lodish, et al. 2008. (Molecular Cell Biology) 6th edition. pg 959 Fig22-7</ref>., also known as XIC. The XIC is located at the centromere and is where decativation of the X Chromosome begins<ref>Hartl.D.L, Ruvolo.M, Genetics: analysis of genes and genomes, eighth edition, Jones and Bartlett Learning, 2012 page 262</ref> This mechanism follows the process of X-inactivation, also termed [[Lyonization|Lyonization]]&nbsp;or single active X principle<span style="line-height: 1.5em;">, in which regardless of the amount of </span>[[X chromosomes|X chromosomes]]<span style="line-height: 1.5em;"> are present, all but one are inactivated. However, although one of the X chromosomes is said to be inactivated, there is still around 15%</span><span style="line-height: 1.5em;">&nbsp;of the genes on the inactivated X chromosome which aren't inactivtaed.&nbsp;<ref>Whitehall Dr S.K, Genetics Lecture 13, BGM1004 lecture, accessed 27/10/14,</ref></span>  
As human females have two [[X chromosome|X chromosomes]], this means they have the ability to produce twice as much X-linked gene product, this Dosage Compensation Mechanism is responsible for&nbsp;keeping levels of the X-linked gene product similar in both males and females. Therefore, such a mechanism only exists in females. Dosage compensation requires [[RNA polymerase|RNA polymerase]], [[Tsix transcript|Tsix transcript]] and [[Xist transcript|Xist transcript]] as well as the X chromosomes of developing embryonic cells. Note that each transcript is transcribed on one [[Chromosome|chromosome]] each. Xist acts as to ensure inactivation of X chromosome whereas Tsix ensures X chromosome remains active. Such activity is carried out from the [[X inactivation centre|X inactivation centre]]&nbsp;<ref>Lodish, et al. 2008. (Molecular Cell Biology) 6th edition. pg 959 Fig22-7</ref>., also known as XIC. The XIC is located at the centromere and is where decativation of the X Chromosome begins<ref>Hartl.D.L, Ruvolo.M, Genetics: analysis of genes and genomes, eighth edition, Jones and Bartlett Learning, 2012 page 262</ref> This mechanism follows the process of X-inactivation, also termed [[Lyonization|Lyonization]]&nbsp;or single active X principle<span style="line-height: 1.5em;">, in which regardless of the amount of </span>[[X chromosomes|X chromosomes]]<span style="line-height: 1.5em;"> are present, all but one are inactivated. However, although one of the X chromosomes is said to be inactivated, there is still around 15%</span><span style="line-height: 1.5em;">&nbsp;of the genes on the inactivated X chromosome which aren't inactivtaed.&nbsp;<ref>Whitehall Dr S.K, Genetics Lecture 13, BGM1004 lecture, accessed 27/10/14,</ref></span>  


=== References ===
=== In other organisms ===


<references />
Dosage compensation in other sexually-reproducing organisms is achieved through other mechanisms. ''Drosophila ''transcribe X chromosome genes in males at twice the level of the female X chromosomes. This increase in transcription is caused by changes in chromatin over the male X chromosome. A dosage-compensation complex forms and brings about this up-regulation. It is associated with histone-modifiying enzymes and two non-coding RNAs transcribed from the male X chromosome.<ref>Conrad, T. and Akhtar, A. (2012). Dosage compensation in Drosophila melanogaster: epigenetic fine-tuning of chromosome-wide transcription. Nat Rev Genet, 13(2), pp.123-134.</ref><ref>Alberts, B., Johnson, A., Lewis, J., Raff, M., Roberts, K. and Walters, P. (2007) Molecular Biology of the Cell 5th ed., New York: Taylor &amp;amp; Francis. pp. 275fckLRfckLRIn the nematode worm, sexes are male and hermaphrodite. Males possess one X chromosome, and hermaphrodites contain two X chromosomes. Dosage compensation comes about through a reduction in transcription on each X chromosome in the hermaphrodite. This down-regulation is two fold and, as in the examples above, results in equal transcription in the two sexes. Here, a dosage-compensation complex, dissimilar to that in ''Drosophila'', forms and each gene is effected. The exact mechanism is unknown.&lt;ref&gt;Ercan, S. and Lieb, J. (2009). C. elegans dosage compensation: A window into mechanisms of domain-scale gene regulation. Chromosome Research, 17(2), pp.215-227.</ref><ref>Alberts, B., Johnson, A., Lewis, J., Raff, M., Roberts, K. and Walters, P. (2007) Molecular Biology of the Cell 5th ed., New York: Taylor &amp;amp; Francis. pp. 275-276fckLRfckLR=== References  ===fckLRfckLR&lt;references /&gt;</ref>

Revision as of 00:23, 28 November 2014

As human females have two X chromosomes, this means they have the ability to produce twice as much X-linked gene product, this Dosage Compensation Mechanism is responsible for keeping levels of the X-linked gene product similar in both males and females. Therefore, such a mechanism only exists in females. Dosage compensation requires RNA polymerase, Tsix transcript and Xist transcript as well as the X chromosomes of developing embryonic cells. Note that each transcript is transcribed on one chromosome each. Xist acts as to ensure inactivation of X chromosome whereas Tsix ensures X chromosome remains active. Such activity is carried out from the X inactivation centre [1]., also known as XIC. The XIC is located at the centromere and is where decativation of the X Chromosome begins[2] This mechanism follows the process of X-inactivation, also termed Lyonization or single active X principle, in which regardless of the amount of X chromosomes are present, all but one are inactivated. However, although one of the X chromosomes is said to be inactivated, there is still around 15% of the genes on the inactivated X chromosome which aren't inactivtaed. [3]

In other organisms

Dosage compensation in other sexually-reproducing organisms is achieved through other mechanisms. Drosophila transcribe X chromosome genes in males at twice the level of the female X chromosomes. This increase in transcription is caused by changes in chromatin over the male X chromosome. A dosage-compensation complex forms and brings about this up-regulation. It is associated with histone-modifiying enzymes and two non-coding RNAs transcribed from the male X chromosome.[4][5][6]

  1. ↑ Lodish, et al. 2008. (Molecular Cell Biology) 6th edition. pg 959 Fig22-7
  2. ↑ Hartl.D.L, Ruvolo.M, Genetics: analysis of genes and genomes, eighth edition, Jones and Bartlett Learning, 2012 page 262
  3. ↑ Whitehall Dr S.K, Genetics Lecture 13, BGM1004 lecture, accessed 27/10/14,
  4. ↑ Conrad, T. and Akhtar, A. (2012). Dosage compensation in Drosophila melanogaster: epigenetic fine-tuning of chromosome-wide transcription. Nat Rev Genet, 13(2), pp.123-134.
  5. ↑ Alberts, B., Johnson, A., Lewis, J., Raff, M., Roberts, K. and Walters, P. (2007) Molecular Biology of the Cell 5th ed., New York: Taylor &amp; Francis. pp. 275fckLRfckLRIn the nematode worm, sexes are male and hermaphrodite. Males possess one X chromosome, and hermaphrodites contain two X chromosomes. Dosage compensation comes about through a reduction in transcription on each X chromosome in the hermaphrodite. This down-regulation is two fold and, as in the examples above, results in equal transcription in the two sexes. Here, a dosage-compensation complex, dissimilar to that in Drosophila, forms and each gene is effected. The exact mechanism is unknown.<ref>Ercan, S. and Lieb, J. (2009). C. elegans dosage compensation: A window into mechanisms of domain-scale gene regulation. Chromosome Research, 17(2), pp.215-227.
  6. ↑ Alberts, B., Johnson, A., Lewis, J., Raff, M., Roberts, K. and Walters, P. (2007) Molecular Biology of the Cell 5th ed., New York: Taylor &amp; Francis. pp. 275-276fckLRfckLR=== References ===fckLRfckLR<references />
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