Fine-structure mapping of the complex locus Odc-rs5 relative to Igk and distal loci

1992 ◽  
Vol 3 (12) ◽  
pp. 689-699 ◽  
Author(s):  
Beverly A. Richards-Smith ◽  
Rosemary W. Elliott
1982 ◽  
Vol 2 (12) ◽  
pp. 1501-1513
Author(s):  
Janet Kurjan ◽  
Benjamin D. Hall

The SUP4 tRNA Tyr locus in Saccharomyces cerevisiae has been studied by the isolation and characterization of mutations at the SUP4 gene which result in the loss of suppressor function. Most of the mutations act as single-site mutations, whereas about a third of the mutations are deletions of the entire gene. Two meiotic fine-structure maps of the gene were made. The first mapping technique placed 10 mutations plus the sup4 + anticodon on a map by a measurement of levels of recombination between pairs of mutations. The second map utilized a more qualitative estimate of recombination frequency, allowing 69 mutations and the sup4 + anticodon to be mapped. The maps were compared with the physical structure of the gene for the 34 mutations whose nucleotide alteration has been determined by DNA sequencing (Koski et al., Cell 22 :415-425, 1980; Kurjan et al., Cell 20 :701-709, 1980). Both maps show a good correlation with the physical structure of the gene, even though certain properties of genetic fine-structure maps, such as marker effects and “map expansion,” were seen.


Genetics ◽  
1982 ◽  
Vol 102 (2) ◽  
pp. 139-147
Author(s):  
Michael J Hynes

ABSTRACT A mutant producing very high levels of the acetamidase enzyme encoded by the amdS gene has been isolated in a strain containing the amdA7 mutation, which itself causes high levels of this enzyme. Genetic analysis has shown that this mutation, designated amdI66, is adjacent to the amdS gene and is cis-dominant in its effect. The amdI66 mutation has little effect on amdS expression when present in strains not containing the amdA7 mutation. Two other amdA mutations investigated also interact with the amdI66 mutation to result in high acetamidase levels. No interaction between amdI66 and any of the other putative regulatory genes affecting amdS expression has been observed. The amdI66 mutation has been located by fine structure mapping at the extreme end of the controlling region, which has previously been defined by genetic mapping (Hynes 1979). Analysis of this region has been extended by mapping new mutations resulting in loss of amdS expression. One of these defines the most extreme site capable of mutation to loss of gene function found so far.


2003 ◽  
Vol 112 (2) ◽  
pp. 209-216 ◽  
Author(s):  
Hal M. Hoffman ◽  
Simon G. Gregory ◽  
James L. Mueller ◽  
Mark Tresierras ◽  
David H. Broide ◽  
...  

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