Difference between revisions of "File:PICH and BLM dependant DNA catenation resolution model.jpg"

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(The model for ultrafine anaphase bridge decatenation, which is dependant on BLM/PICH proteins which allow for the topoisomerase IIa to bind and cut the DNA. If topo IIa does not carry out its job successfully, centromeric nondisjunction may result, as ...)
 
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The model for ultrafine anaphase bridge decatenation, which is dependant on BLM/PICH proteins which allow for the topoisomerase IIa to bind and cut the DNA. If topo IIa does not carry out its job successfully, centromeric nondisjunction may result, as well as the creation of more ultrafine anaphase bridges.
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Title: Model for ultrafine anaphase bridge PICH/BLM dependant decatenation
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Comment: The model for ultrafine anaphase bridge decatenation, which is dependant on BLM/PICH proteins which allow for the topoisomerase IIa to bind and cut the DNA. If topo IIa does not carry out its job successfully, centromeric nondisjunction may result, as well as the creation of more ultrafine anaphase bridges.
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Original figure legend: Model of PICH/BLM-dependent decatenation of centromeric DNA.
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===Reference===
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<ref><pubmed>22563370</pubmed></ref>
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===Copyright===
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Copyright Rouzeau et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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{{Student Image}}
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Original image file name: pone.0033905.g006
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Web address: http://www.ncbi.nlm.nih.gov/pubmed/22563370
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Paper title: Bloom's syndrome and PICH helicases cooperate with topoisomerase IIα in centromere disjunction before anaphase.
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Figure legend: We propose that the combined action of BLM and PICH promotes the organization of centromeric chromatin, thereby rendering some centromeric catenates accessible to Topo IIα. In the absence of BLM or PICH, a defect in the recruitment of active Topo IIα results in the persistence of some catenations leading to centromeric non disjunction and the formation of additional UFBs.
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==References==
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<references/>

Revision as of 13:11, 16 May 2013

Title: Model for ultrafine anaphase bridge PICH/BLM dependant decatenation

Comment: The model for ultrafine anaphase bridge decatenation, which is dependant on BLM/PICH proteins which allow for the topoisomerase IIa to bind and cut the DNA. If topo IIa does not carry out its job successfully, centromeric nondisjunction may result, as well as the creation of more ultrafine anaphase bridges.

Original figure legend: Model of PICH/BLM-dependent decatenation of centromeric DNA.

Reference

[1]

Copyright

Copyright Rouzeau et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Note - This image was originally uploaded as part of a student project and may contain inaccuracies in either description or acknowledgements. Please contact the site coordinator if the uploaded content does not meet the original copyright permission or requirements, for immediate removal.

Original image file name: pone.0033905.g006

Web address: http://www.ncbi.nlm.nih.gov/pubmed/22563370

Paper title: Bloom's syndrome and PICH helicases cooperate with topoisomerase IIα in centromere disjunction before anaphase.

Figure legend: We propose that the combined action of BLM and PICH promotes the organization of centromeric chromatin, thereby rendering some centromeric catenates accessible to Topo IIα. In the absence of BLM or PICH, a defect in the recruitment of active Topo IIα results in the persistence of some catenations leading to centromeric non disjunction and the formation of additional UFBs.

References

  1. <pubmed>22563370</pubmed>

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