PMID:11459954 - Revision history

imported>Wikientrybot: change PMID template to TableEdit version

2013-09-15T04:15:22Z

change PMID template to TableEdit version

← Older revision		Revision as of 04:15, 15 September 2013
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	!align=left \|Citation		!align=left \|Citation
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	'''~~No author listed~~''' (2001) Effects of mutations involving cell division, recombination, and chromosome dimer resolution on a priA2::kan mutant. ''Proc. Natl. Acad. Sci. U.S.A.'' '''98''':8203-10		'''McCool, JD and Sandler, SJ''' (2001) Effects of mutations involving cell division, recombination, and chromosome dimer resolution on a priA2::kan mutant. ''Proc. Natl. Acad. Sci. U.S.A.'' '''98''':8203-10
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	!align=left \|Abstract		!align=left \|Abstract

imported>Wikientrybot: replace GO_table_reference with annotationlinks

2013-09-01T18:03:40Z

replace GO_table_reference with annotationlinks

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 ==Annotations {{HelpIcon|Help:Literature}}==
-<!--box uid=63ce1649aab8b3180235b0af7618f667.0.S47ab957461378-->
+<annotationlinks/>
 ==EcoliWiki Links {{HelpIcon|Help:Literature}} ==

imported>Wikientrybot: change PMID template to TableEdit version

2013-09-01T18:03:40Z

change PMID template to TableEdit version

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-|{{TableHeadingColor}} |'''Abstract''' || Recombinational repair of replication forks can occur either to a crossover (XO) or noncrossover (non-XO) depending on Holliday junction resolution. Once the fork is repaired by recombination, PriA is important for restarting these forks in Escherichia coli. PriA mutants are Rec(-) and UV sensitive and have poor viability and 10-fold elevated basal levels of SOS expression. PriA sulB mutant cells and their nucleoids were studied by differential interference contrast and fluorescence microscopy of 4',6-diamidino-2-phenylindole-stained log phase cells. Two populations of cells were seen. Eighty four percent appeared like wild type, and 16% of the cells were filamented and had poorly partitioned chromosomes (Par(-)). To probe potential mechanisms leading to the two populations of cells, mutations were added to the priA sulB mutant. Mutating sulA or introducing lexA3 decreased, but did not eliminate filamentation or defects in partitioning. Mutating either recA or recB virtually eliminated the Par(-) phenotype. Filamentation in the recB mutant decreased to 3%, but increased to 28% in the recA mutant. The ability to resolve and/or branch migrate Holliday junctions also appeared crucial in the priA mutant because removing either recG or ruvC was lethal. Lastly, it was tested whether the ability to resolve chromosome dimers caused by XOs was important in a priA mutant by mutating dif and the C-terminal portion of ftsK. Mutation of dif showed no change in phenotype whereas ftsK1cat was lethal with priA2kan. A model is proposed where the PriA-independent pathway of replication restart functions at forks that have been repaired to non-XOs.
+!align=left  |Citation
-</noinclude>
+||
 |-
-|{{TableHeadingColor}} nowrap |'''Links''' ||  [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11459954 PubMed]
+!align=left  |Keywords
 |}
+<!--box uid=d41d8cd98f00b204e9800998ecf8427e.133237.H5223817c5a926-->
 ==Significance {{HelpIcon|Help:Literature}} ==
 {{LitSignificance}}

127.0.0.1: /Volumes/r3/t3/ul/working/touchTables/touch_all_tables.php

2010-06-17T19:56:46Z

/Volumes/r3/t3/ul/working/touchTables/touch_all_tables.php

← Older revision		Revision as of 19:56, 17 June 2010
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	{\| id="S47ab957461378" class=" tableEdit GO_table_reference"		{\| id="S47ab957461378" class=" tableEdit GO_table_reference"
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	!\|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status		!\|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

127.0.0.1: Update TableEdit tables.

2010-01-09T03:55:45Z

Update TableEdit tables.

← Older revision		Revision as of 03:55, 9 January 2010
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	\|- ~~{{table heading style}}~~		\|-
	!\|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status		!\|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

	\|-class=~~'sortbottom'~~		\|- class="tableEdit_footer"
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imported>Wikientrybot: Fix links due to TableEditLinks.php changes.

2009-02-20T00:05:18Z

Fix links due to TableEditLinks.php changes.

← Older revision		Revision as of 00:05, 20 February 2009
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	* PLEASE DON'T EDIT THIS TABLE DIRECTLY. Use the edit table link under the table.		* PLEASE DON'T EDIT THIS TABLE DIRECTLY. Use the edit table link under the table.
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	\|- {{table heading style}}		\|- {{table heading style}}
	!Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status		!\|Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status

	\|-class='sortbottom'		\|-class='sortbottom'
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127.0.0.1: Edited by wikibot

2008-04-30T13:11:29Z

Edited by wikibot

← Older revision		Revision as of 13:11, 30 April 2008
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	!Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status		!Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status
	\|-class='sortbottom'		\|-class='sortbottom'
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127.0.0.1: Edited by wikibot

2008-04-25T22:49:42Z

Edited by wikibot

← Older revision		Revision as of 22:49, 25 April 2008
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	\|{{TableHeadingColor}} nowrap \|'''Links''' \|\| [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11459954 PubMed]		\|{{TableHeadingColor}} nowrap \|'''Links''' \|\| [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11459954 PubMed]
	\|}		\|}
	~~</protect>~~
	==Significance {{HelpIcon\|Help:Literature}} ==		==Significance {{HelpIcon\|Help:Literature}} ==
	{{LitSignificance}}		{{LitSignificance}}
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	==Annotations {{HelpIcon\|Help:Literature}}==		==Annotations {{HelpIcon\|Help:Literature}}==
	~~<protect>~~<!--box uid=63ce1649aab8b3180235b0af7618f667.0.S47ab957461378-->		<!--box uid=63ce1649aab8b3180235b0af7618f667.0.S47ab957461378-->
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	==EcoliWiki Links {{HelpIcon\|Help:Literature}} ==		==EcoliWiki Links {{HelpIcon\|Help:Literature}} ==

165.91.10.100: New PMID: Page!

2008-02-07T23:34:12Z

New PMID: Page!

New page

<protect>
{{RightTOC}}

<span style = 'font-size: large'> '''McCool, JD and Sandler, SJ''' (2001) Effects of mutations involving cell division, recombination, and chromosome dimer resolution on a priA2::kan mutant.''Proc. Natl. Acad. Sci. U.S.A.'' '''98''':8203-10</span>

{|{{Prettytable}} align = 'center' width= '70%'
|-
|{{TableHeadingColor}} |'''Abstract''' || Recombinational repair of replication forks can occur either to a crossover (XO) or noncrossover (non-XO) depending on Holliday junction resolution. Once the fork is repaired by recombination, PriA is important for restarting these forks in Escherichia coli. PriA mutants are Rec(-) and UV sensitive and have poor viability and 10-fold elevated basal levels of SOS expression. PriA sulB mutant cells and their nucleoids were studied by differential interference contrast and fluorescence microscopy of 4',6-diamidino-2-phenylindole-stained log phase cells. Two populations of cells were seen. Eighty four percent appeared like wild type, and 16% of the cells were filamented and had poorly partitioned chromosomes (Par(-)). To probe potential mechanisms leading to the two populations of cells, mutations were added to the priA sulB mutant. Mutating sulA or introducing lexA3 decreased, but did not eliminate filamentation or defects in partitioning. Mutating either recA or recB virtually eliminated the Par(-) phenotype. Filamentation in the recB mutant decreased to 3%, but increased to 28% in the recA mutant. The ability to resolve and/or branch migrate Holliday junctions also appeared crucial in the priA mutant because removing either recG or ruvC was lethal. Lastly, it was tested whether the ability to resolve chromosome dimers caused by XOs was important in a priA mutant by mutating dif and the C-terminal portion of ftsK. Mutation of dif showed no change in phenotype whereas ftsK1cat was lethal with priA2kan. A model is proposed where the PriA-independent pathway of replication restart functions at forks that have been repaired to non-XOs.
</noinclude>
|-
|{{TableHeadingColor}} nowrap |'''Links''' || [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11459954 PubMed]
|}
</protect>
==Significance {{HelpIcon|Help:Literature}} ==
{{LitSignificance}}

== Useful Materials and Methods {{HelpIcon|Help:Literature}}==
{{LitMaterials}}

==Annotations {{HelpIcon|Help:Literature}}==
<protect>

{|class = 'sortable' {{Prettytable}} id='241061'
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!Gene product!!Qualifier!!GO ID!!GO term name!!Evidence Code!!with/from!!Aspect!!Notes!!Status
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==EcoliWiki Links {{HelpIcon|Help:Literature}} ==
{{LitLinks}}

==References==
{{RefHelp}}
<references/>