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Genomic organization in Caenorhabditis elegans: deficiency mapping on linkage group V(left)

Published online by Cambridge University Press:  14 April 2009

Raja E. Rosenbluth,
Teresa M. Rogalski,
Robert C. Johnsen,
Linda M. Addison and
David L. Baillie
Raja E. Rosenbluth*
Affiliation:
Department of Biological Sciences, Simon Fraser University, Burnaby, B.C., Canada V5A 1S6
Teresa M. Rogalski
Affiliation:
Department of Biological Sciences, Simon Fraser University, Burnaby, B.C., Canada V5A 1S6
Robert C. Johnsen
Affiliation:
Department of Biological Sciences, Simon Fraser University, Burnaby, B.C., Canada V5A 1S6
Linda M. Addison
Affiliation:
Department of Biological Sciences, Simon Fraser University, Burnaby, B.C., Canada V5A 1S6
David L. Baillie
Affiliation:
Department of Biological Sciences, Simon Fraser University, Burnaby, B.C., Canada V5A 1S6
*
† Corresponding author.
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In this study we genetically analyse a large autosomal region (23 map units) in Caenorhabditis elegans. The region comprises the left half of linkage group V [LGV(left)] and is recombinationally balanced by the translocation eT1(III; V). We have used rearrangement breakpoints to subdivide the region from the left end of LGV to daf-11 into a set of 23 major zones. Twenty of these zones are balanced by eT1. To establish the zones we examined a total of 110 recessive lethal mutations derived from a variety of screening protocols. The mutations identified 12 deficiencies, 1 duplication, as well as 98 mutations that fell into 59 complementation groups, significantly increasing the number of available genetic sites on LGV. Twenty-six of the latter had more than 1 mutant allele. Significant differences were observed among the alleles of only 6 genes, 3 of which have at least one ‘visible’ allele. Several deficiencies and 3 alleles of let-336 were demonstrated to affect recombination. The duplication identified in this study is sDp30(V;X). Lethal mutations covered by sDp30 were not suppressed uniformly in hermaphrodites. The basis for this non-uniformity may be related to the mechanism of X chromosome dosage compensation in C. elegans.

Information

Type
Research Article
Information
Genetics Research , Volume 52 , Issue 2 , October 1988, pp. 105 - 118
Copyright
Copyright © Cambridge University Press 1988

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