Genetic and biochemical study of threonine-overproducing mutants of Saccharomyces cerevisiae
Three threonine-overproducing mutants were obtained as prototrophic revertants of a hom3 mutant strain of Saccharomyces cerevisiae. The gene HOM3 codes for aspartokinase (aspartate kinase; EC 2.7.2.4), the first enzyme of the threonine-methionine biosynthetic route, which is subjected to feedback in...
| Authors: | , , |
|---|---|
| Format: | article |
| Status: | Published version |
| Publication Date: | 1982 |
| Country: | España |
| Institution: | Universidad de Sevilla (US) |
| Repository: | idUS. Depósito de Investigación de la Universidad de Sevilla |
| OAI Identifier: | oai:idus.us.es:11441/70789 |
| Online Access: | https://hdl.handle.net/11441/70789 https://doi.org/10.1128/MCB.2.7.731 |
| Access Level: | Open access |
| Keyword: | Saccharomyces cerevisiae Threonine Aspartate kinasethreonine |
| Summary: | Three threonine-overproducing mutants were obtained as prototrophic revertants of a hom3 mutant strain of Saccharomyces cerevisiae. The gene HOM3 codes for aspartokinase (aspartate kinase; EC 2.7.2.4), the first enzyme of the threonine-methionine biosynthetic route, which is subjected to feedback inhibition by threonine. Enzymatic studies indicated that aspartokinase from the revertants has lost the feedback inhibition, resulting in overproduction of threonine. These revertants also bore one or two additional mutations, named texl-J and tex2-1, which alone or jointly made possible the excretion of the threonine accumulated. The effect of these two genes on excretion is potentiated by excess inositol in the medium. |
|---|