Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

The two yeast mating-type alleles MATa and MAT alpha each produce two mRNAs that are transcribed in opposite and diverging directions from central promoters. Silent copies of MATa (HMRa) and MAT alpha (HML alpha) contain identical DNA sequences throughout the transcribed region, yet are not transcribed, except in sir- strains. Since SIR represses not only transcription from a silent copy but also its ability to act as a recipient in a mating-type interconversion, we have investigated whether it might act by regulating the entire chromatin structure of a silent locus. We have therefore compared the profile of DNAase I and micrococcal nuclease cleavage at HML alpha with MAT alpha and HMRa with MATa in sir- and SIR+ strains. We find that SIR is necessary for the maintenance of a different chromatin structure at HM loci from their active counterparts at MAT. One particularly striking change that SIR induces provides a simple explanation for one of its biological properties: control of directionality of switching. SIR causes the disappearance of a DNAase I-hypersensitive site at Y-Z boundary (found at MAT or HM sir-) that is coincident with a double-strand cleavage possibly created by HO in the initiation of a mating-type switch.

Type

Journal article

Journal

Cell

Publication Date

09/1982

Volume

30

Pages

567 - 578

Keywords

Base Sequence, Chromatin, Chromosome Mapping, Crosses, Genetic, Deoxyribonuclease I, Endodeoxyribonucleases, Gene Expression Regulation, Genes, Regulator, Micrococcal Nuclease, Mutation, Saccharomyces cerevisiae, Transcription, Genetic