RESUMEN
The problem of mating-type switches in heterothallic yeast cells was investigated. In selective system for cytoduction in alpha x alpha crosses alpha-cytoductants were predominantly obtained. Thus matings in alpha x alpha crosses can proceed through non-heritable changes (modifications) of the mating type alpha----a. The frequency of alpha-cytoductants after UV-irradiation of the recipient cells exceeded the control value 50-90 times. The extra copy of MAT alpha dramatically decreased the frequency of cytoductants in alpha x alpha crosses, either spontaneously or after UV-irradiation. The rad18 recipient defective in postreplication repair had 70-times increased level of mating-type modifications, as compared with isogenic Rad+ strain. An explanation consistent with these data is that mating-type modifications are due to phenotypic expression of primary lesions of MAT alpha locus. Such lesions might be expressed as transient a-mating type. After the mating event, these lesions can be repaired or turned to true mutations within the MAT locus. In fact, approximately half of non-mating cytoductants from alpha x alpha crosses had the phenotype of mat alpha 2 mutants.
Asunto(s)
ADN de Hongos/genética , Saccharomyces cerevisiae/genética , Mapeo Cromosómico , Clonación Molecular , Medios de Cultivo , ADN de Hongos/efectos de la radiación , Marcadores Genéticos , Haploidia , Mutación , Hibridación de Ácido Nucleico , Fenotipo , Plásmidos , Transformación Genética , Rayos UltravioletaRESUMEN
Expression of the yeast LEU2 gene in Escherichia coli is not sufficiently high. That is why the growth rate of leuB E. coli transformants slowed down on media lacking leucine. The mutations leading to the increase in yeast gene expression in bacteria were found. It has been shown that mutations are connected with insertion of the bacterial IS1 element into the regulatory region of LEU2. The increase in the yeast gene expression does not depend on orientation of the inserted IS1 element. The IS1 element insertion seems to control the attenuation of transcription of LEU2.