scholarly journals Reciprocal Crossovers and a Positional Preference for Strand Exchange in Recombination Events Resulting in Deletion or Duplication of Chromosome 17p11.2

2003 ◽  
Vol 73 (6) ◽  
pp. 1302-1315 ◽  
Author(s):  
Weimin Bi ◽  
Sung-Sup Park ◽  
Christine J. Shaw ◽  
Marjorie A. Withers ◽  
Pragna I. Patel ◽  
...  
Keyword(s):  
Strand Exchange ◽  
Positional Preference

Yeastspt6-140Mutation, Affecting Chromatin and Transcription, Preferentially Increases Recombination in Which Rad51p-Mediated Strand Exchange Is Dispensable

Genetics ◽  
2001 ◽  
Vol 158 (2) ◽  
pp. 597-611 ◽  
Author(s):  
Francisco Malagón ◽  
Andrés Aguilera
Keyword(s):  
Strand Exchange ◽  
Micrococcal Nuclease ◽  
Sensitivity Analyses ◽  
Inverted Repeats ◽  
Major Mechanism ◽  
Spontaneous Recombination ◽  
Single Strand Annealing ◽  
Strand Invasion ◽  
Strand Annealing ◽  
Break Induced Replication

AbstractWe have shown that the spt6-140 and spt4-3 mutations, affecting chromatin structure and transcription, stimulate recombination between inverted repeats by a RAD52-dependent mechanism that is very efficient in the absence of RAD51, RAD54, RAD55, and RAD57. Such a mechanism of recombination is RAD1-RAD59-dependent and yields gene conversions highly associated with the inversion of the repeat. The spt6-140 mutation alters transcription and chromatin in our inverted repeats, as determined by Northern and micrococcal nuclease sensitivity analyses, respectively. Hyper-recombination levels are diminished in the absence of transcription. We believe that the chromatin alteration, together with transcription impairment caused by spt6-140, increases the incidence of spontaneous recombination regardless of whether or not it is mediated by Rad51p-dependent strand exchange. Our results suggest that spt6, as well as spt4, primarily stimulates a mechanism of break-induced replication. We discuss the possibility that the chromatin alteration caused by spt6-140 facilitates a Rad52p-mediated one-ended strand invasion event, possibly inefficient in wild-type chromatin. Our results are consistent with the idea that the major mechanism leading to inversions might not be crossing over but break-induced replication followed by single-strand annealing.

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