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VERMILION-DEFICIENCY
In May, 1916, a culture of Drosophila melanogaster showed that a new sex-linked lethal had arisen. The linkage relations indicated that the position of the lethal was in the neighborhood of the sex-linked recessive "vermilion," whose locus in the X chromosome is at 33.0. When females heter...
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Formato: | Texto |
Lenguaje: | English |
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The Rockefeller University Press
1919
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2140334/ https://www.ncbi.nlm.nih.gov/pubmed/19871779 |
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author | Bridges, Calvin B. |
author_facet | Bridges, Calvin B. |
author_sort | Bridges, Calvin B. |
collection | PubMed |
description | In May, 1916, a culture of Drosophila melanogaster showed that a new sex-linked lethal had arisen. The linkage relations indicated that the position of the lethal was in the neighborhood of the sex-linked recessive "vermilion," whose locus in the X chromosome is at 33.0. When females heterozygous for the lethal were outcrossed to vermilion males, all the daughters that received the lethal-bearing chromosome showed vermilion eye-color, though, from the pedigree, vermilion was known to be absent from the ancestry of the mother. The lethal action and the unexpected appearance of vermilion both suggested that this was another instance of the phenomenon called "deficiency;" that is, the loss or "inactivation" of the genes of a section of the X chromosome. The lethal action would then be due to the deficient region including one or more genes necessary for the life of the individual. The appearance of vermilion in females carrying only one vermilion gene would be explainable on the ground that the deficient-bearing females are virtually haploid for the region including the vermilion locus. Linkage tests showed that the amount of crossing over in the neighborhood of the deficiency was cut down by about five units. Part of this may be attributed to the actual length of the "deficient" region, within which it is probable that no crossing over occurs, and part (probably most) to an alteration in the synaptic relations in the regions immediately adjacent. In more remote regions there was no disturbance or perhaps a slight rise in the frequency of crossing over. Both the local fall and the possible rise in more distant regions would seem to argue that a "pucker" at synapsis had been caused by an actual shortening of the deficient chromosome. That the deficient region extends to the left of the locus of vermilion was indicated by a test in which it was observed that the presence of an extra piece of chromosome including the loci for vermilion and sable ("vermilion-sable duplication") did not neutralize the lethal action of the deficiency. Haploid tests with the other recessive mutations in the neighborhood of vermilion showed that the deficiency was not extensive enough to include their loci. Cytological preparations were made but were unsatisfactory. The stock was finally lost, apparently as the result of injurious action upon viability, fertility, and productivity by the deficiency. |
format | Text |
id | pubmed-2140334 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1919 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21403342008-04-23 VERMILION-DEFICIENCY Bridges, Calvin B. J Gen Physiol Article In May, 1916, a culture of Drosophila melanogaster showed that a new sex-linked lethal had arisen. The linkage relations indicated that the position of the lethal was in the neighborhood of the sex-linked recessive "vermilion," whose locus in the X chromosome is at 33.0. When females heterozygous for the lethal were outcrossed to vermilion males, all the daughters that received the lethal-bearing chromosome showed vermilion eye-color, though, from the pedigree, vermilion was known to be absent from the ancestry of the mother. The lethal action and the unexpected appearance of vermilion both suggested that this was another instance of the phenomenon called "deficiency;" that is, the loss or "inactivation" of the genes of a section of the X chromosome. The lethal action would then be due to the deficient region including one or more genes necessary for the life of the individual. The appearance of vermilion in females carrying only one vermilion gene would be explainable on the ground that the deficient-bearing females are virtually haploid for the region including the vermilion locus. Linkage tests showed that the amount of crossing over in the neighborhood of the deficiency was cut down by about five units. Part of this may be attributed to the actual length of the "deficient" region, within which it is probable that no crossing over occurs, and part (probably most) to an alteration in the synaptic relations in the regions immediately adjacent. In more remote regions there was no disturbance or perhaps a slight rise in the frequency of crossing over. Both the local fall and the possible rise in more distant regions would seem to argue that a "pucker" at synapsis had been caused by an actual shortening of the deficient chromosome. That the deficient region extends to the left of the locus of vermilion was indicated by a test in which it was observed that the presence of an extra piece of chromosome including the loci for vermilion and sable ("vermilion-sable duplication") did not neutralize the lethal action of the deficiency. Haploid tests with the other recessive mutations in the neighborhood of vermilion showed that the deficiency was not extensive enough to include their loci. Cytological preparations were made but were unsatisfactory. The stock was finally lost, apparently as the result of injurious action upon viability, fertility, and productivity by the deficiency. The Rockefeller University Press 1919-07-20 /pmc/articles/PMC2140334/ /pubmed/19871779 Text en Copyright © Copyright, 1919, by The Rockefeller Institute for Medical Research This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Article Bridges, Calvin B. VERMILION-DEFICIENCY |
title | VERMILION-DEFICIENCY |
title_full | VERMILION-DEFICIENCY |
title_fullStr | VERMILION-DEFICIENCY |
title_full_unstemmed | VERMILION-DEFICIENCY |
title_short | VERMILION-DEFICIENCY |
title_sort | vermilion-deficiency |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2140334/ https://www.ncbi.nlm.nih.gov/pubmed/19871779 |
work_keys_str_mv | AT bridgescalvinb vermiliondeficiency |