1mg7

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(New page: 200px<br /><applet load="1mg7" size="450" color="white" frame="true" align="right" spinBox="true" caption="1mg7, resolution 1.55&Aring;" /> '''Crystal Structure of...)
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[[Image:1mg7.gif|left|200px]]<br /><applet load="1mg7" size="350" color="white" frame="true" align="right" spinBox="true"
caption="1mg7, resolution 1.55&Aring;" />
caption="1mg7, resolution 1.55&Aring;" />
'''Crystal Structure of xol-1'''<br />
'''Crystal Structure of xol-1'''<br />
==Overview==
==Overview==
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In Caenorhabditis elegans, an X chromosome-counting mechanism specifies, sexual fate. Specific genes termed X-signal elements, which are present on, the X chromosome, act in a concerted dose-dependent fashion to regulate, levels of the developmental switch gene xol-1. In turn, xol-1 levels, determine sexual fate and the activation state of the dosage compensation, mechanism. The crystal structure of the XOL-1 protein at 1.55 A resolution, unexpectedly reveals that xol-1 encodes a GHMP kinase family member, despite sequence identity of 10% or less. Because GHMP kinases, thus far, have only been characterized as small molecule kinases involved in, metabolic pathways, for example, amino acid and cholesterol synthesis, XOL-1 is the first member that controls nonmetabolic processes., Biochemical investigations demonstrated that XOL-1 does not bind ATP under, standard conditions, suggesting that XOL-1 acts by a mechanism distinct, from that of other GHMP kinases. In addition, we have cloned a XOL-1, ortholog from Caenorhabditis briggsae, a related nematode that diverged, from C. elegans approximately 50-100 million years ago. These findings, demonstrate an unanticipated role for GHMP kinase family members as, mediators of sexual differentiation and dosage compensation and, possibly, other aspects of differentiation and development.
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In Caenorhabditis elegans, an X chromosome-counting mechanism specifies sexual fate. Specific genes termed X-signal elements, which are present on the X chromosome, act in a concerted dose-dependent fashion to regulate levels of the developmental switch gene xol-1. In turn, xol-1 levels determine sexual fate and the activation state of the dosage compensation mechanism. The crystal structure of the XOL-1 protein at 1.55 A resolution unexpectedly reveals that xol-1 encodes a GHMP kinase family member, despite sequence identity of 10% or less. Because GHMP kinases, thus far, have only been characterized as small molecule kinases involved in metabolic pathways, for example, amino acid and cholesterol synthesis, XOL-1 is the first member that controls nonmetabolic processes. Biochemical investigations demonstrated that XOL-1 does not bind ATP under standard conditions, suggesting that XOL-1 acts by a mechanism distinct from that of other GHMP kinases. In addition, we have cloned a XOL-1 ortholog from Caenorhabditis briggsae, a related nematode that diverged from C. elegans approximately 50-100 million years ago. These findings demonstrate an unanticipated role for GHMP kinase family members as mediators of sexual differentiation and dosage compensation and, possibly, other aspects of differentiation and development.
==About this Structure==
==About this Structure==
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1MG7 is a [http://en.wikipedia.org/wiki/Single_protein Single protein] structure of sequence from [http://en.wikipedia.org/wiki/Caenorhabditis_elegans Caenorhabditis elegans]. Full crystallographic information is available from [http://ispc.weizmann.ac.il/oca-bin/ocashort?id=1MG7 OCA].
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1MG7 is a [http://en.wikipedia.org/wiki/Single_protein Single protein] structure of sequence from [http://en.wikipedia.org/wiki/Caenorhabditis_elegans Caenorhabditis elegans]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1MG7 OCA].
==Reference==
==Reference==
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[[Category: Single protein]]
[[Category: Single protein]]
[[Category: Godzik, A.]]
[[Category: Godzik, A.]]
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[[Category: Hassig, C.A.]]
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[[Category: Hassig, C A.]]
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[[Category: Luz, J.G.]]
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[[Category: Luz, J G.]]
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[[Category: Meyer, B.J.]]
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[[Category: Meyer, B J.]]
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[[Category: Wilson, I.A.]]
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[[Category: Wilson, I A.]]
[[Category: alpha-beta]]
[[Category: alpha-beta]]
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''Page seeded by [http://ispc.weizmann.ac.il/oca OCA ] on Tue Nov 20 21:23:55 2007''
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''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Thu Feb 21 13:54:58 2008''

Revision as of 11:54, 21 February 2008


1mg7, resolution 1.55Å

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Crystal Structure of xol-1

Overview

In Caenorhabditis elegans, an X chromosome-counting mechanism specifies sexual fate. Specific genes termed X-signal elements, which are present on the X chromosome, act in a concerted dose-dependent fashion to regulate levels of the developmental switch gene xol-1. In turn, xol-1 levels determine sexual fate and the activation state of the dosage compensation mechanism. The crystal structure of the XOL-1 protein at 1.55 A resolution unexpectedly reveals that xol-1 encodes a GHMP kinase family member, despite sequence identity of 10% or less. Because GHMP kinases, thus far, have only been characterized as small molecule kinases involved in metabolic pathways, for example, amino acid and cholesterol synthesis, XOL-1 is the first member that controls nonmetabolic processes. Biochemical investigations demonstrated that XOL-1 does not bind ATP under standard conditions, suggesting that XOL-1 acts by a mechanism distinct from that of other GHMP kinases. In addition, we have cloned a XOL-1 ortholog from Caenorhabditis briggsae, a related nematode that diverged from C. elegans approximately 50-100 million years ago. These findings demonstrate an unanticipated role for GHMP kinase family members as mediators of sexual differentiation and dosage compensation and, possibly, other aspects of differentiation and development.

About this Structure

1MG7 is a Single protein structure of sequence from Caenorhabditis elegans. Full crystallographic information is available from OCA.

Reference

XOL-1, primary determinant of sexual fate in C. elegans, is a GHMP kinase family member and a structural prototype for a class of developmental regulators., Luz JG, Hassig CA, Pickle C, Godzik A, Meyer BJ, Wilson IA, Genes Dev. 2003 Apr 15;17(8):977-90. Epub 2003 Apr 2. PMID:12672694

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