Genetic interactions involving five or more genes contribute to a complex trait in yeast.
Recent research suggests that genetic interactions involving more than two loci may influence a number of complex traits. How these 'higher-order' interactions arise at the genetic and molecular levels remains an open question. To provide insights into this problem, we dissected a colony m...
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2014-05-01
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| Series: | PLoS Genetics |
| Online Access: | https://journals.plos.org/plosgenetics/article/file?id=10.1371/journal.pgen.1004324&type=printable |
| _version_ | 1826587387976744960 |
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| author | Matthew B Taylor Ian M Ehrenreich |
| author_facet | Matthew B Taylor Ian M Ehrenreich |
| author_sort | Matthew B Taylor |
| collection | DOAJ |
| description | Recent research suggests that genetic interactions involving more than two loci may influence a number of complex traits. How these 'higher-order' interactions arise at the genetic and molecular levels remains an open question. To provide insights into this problem, we dissected a colony morphology phenotype that segregates in a yeast cross and results from synthetic higher-order interactions. Using backcrossing and selective sequencing of progeny, we found five loci that collectively produce the trait. We fine-mapped these loci to 22 genes in total and identified a single gene at each locus that caused loss of the phenotype when deleted. Complementation tests or allele replacements provided support for functional variation in these genes, and revealed that pre-existing genetic variants and a spontaneous mutation interact to cause the trait. The causal genes have diverse functions in endocytosis (END3), oxidative stress response (TRR1), RAS-cAMP signalling (IRA2), and transcriptional regulation of multicellular growth (FLO8 and MSS11), and for the most part have not previously been shown to exhibit functional relationships. Further efforts uncovered two additional loci that together can complement the non-causal allele of END3, suggesting that multiple genotypes in the cross can specify the same phenotype. Our work sheds light on the complex genetic and molecular architecture of higher-order interactions, and raises questions about the broader contribution of such interactions to heritable trait variation. |
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| format | Article |
| id | doaj.art-f6b12b62cfae42e8982c5e062e3042d3 |
| institution | Directory Open Access Journal |
| issn | 1553-7390 1553-7404 |
| language | English |
| last_indexed | 2025-03-14T16:24:38Z |
| publishDate | 2014-05-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS Genetics |
| spelling | doaj.art-f6b12b62cfae42e8982c5e062e3042d32025-02-22T05:31:55ZengPublic Library of Science (PLoS)PLoS Genetics1553-73901553-74042014-05-01105e100432410.1371/journal.pgen.1004324Genetic interactions involving five or more genes contribute to a complex trait in yeast.Matthew B TaylorIan M EhrenreichRecent research suggests that genetic interactions involving more than two loci may influence a number of complex traits. How these 'higher-order' interactions arise at the genetic and molecular levels remains an open question. To provide insights into this problem, we dissected a colony morphology phenotype that segregates in a yeast cross and results from synthetic higher-order interactions. Using backcrossing and selective sequencing of progeny, we found five loci that collectively produce the trait. We fine-mapped these loci to 22 genes in total and identified a single gene at each locus that caused loss of the phenotype when deleted. Complementation tests or allele replacements provided support for functional variation in these genes, and revealed that pre-existing genetic variants and a spontaneous mutation interact to cause the trait. The causal genes have diverse functions in endocytosis (END3), oxidative stress response (TRR1), RAS-cAMP signalling (IRA2), and transcriptional regulation of multicellular growth (FLO8 and MSS11), and for the most part have not previously been shown to exhibit functional relationships. Further efforts uncovered two additional loci that together can complement the non-causal allele of END3, suggesting that multiple genotypes in the cross can specify the same phenotype. Our work sheds light on the complex genetic and molecular architecture of higher-order interactions, and raises questions about the broader contribution of such interactions to heritable trait variation.https://journals.plos.org/plosgenetics/article/file?id=10.1371/journal.pgen.1004324&type=printable |
| spellingShingle | Matthew B Taylor Ian M Ehrenreich Genetic interactions involving five or more genes contribute to a complex trait in yeast. PLoS Genetics |
| title | Genetic interactions involving five or more genes contribute to a complex trait in yeast. |
| title_full | Genetic interactions involving five or more genes contribute to a complex trait in yeast. |
| title_fullStr | Genetic interactions involving five or more genes contribute to a complex trait in yeast. |
| title_full_unstemmed | Genetic interactions involving five or more genes contribute to a complex trait in yeast. |
| title_short | Genetic interactions involving five or more genes contribute to a complex trait in yeast. |
| title_sort | genetic interactions involving five or more genes contribute to a complex trait in yeast |
| url | https://journals.plos.org/plosgenetics/article/file?id=10.1371/journal.pgen.1004324&type=printable |
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