Send to

Choose Destination
EMBO J. 1987 Jan;6(1):243-8.

The determination of mother cell-specific mating type switching in yeast by a specific regulator of HO transcription.

Author information

Medical Research Council, Laboratory of Molecular Biology, Hills Road, Cambridge CB2 2QH, UK.


In haploid homothallic budding yeast, cell division gives rise to a mother cell which proceeds to switch its mating type and a daughter cell (the bud) which does not. Switching is initiated by a specific double strand cleavage of mating type DNA by an endonuclease encoded by the HO gene. Previous data suggest that the pattern of HO transcription is responsible for the mother cell specificity of switching. HO is transcribed transiently, at START, during the cell cycle of mother cells but not at all during the cell cycle of daughter cells. The HO promoter is complex. Sequences between -1000 and -1400 (called URS1) are essential for transcription, whereas sequences between -150 and -900 (called URS2) are necessary for cell cycle control. Moreover, 10 trans-acting gene products called SWI1-10 are necessary for maximum expression. In an attempt to identify the cis-acting DNA sequences which are responsible for mother cell specificity and to identify which SW1 genes are involved, a hybrid GAL/HO promoter was constructed in which the upstream activation region putatively involved in mother cell-specific activation (URS1) is replaced by the upstream activation region of the GAL1-10 promoter. The properties of this hybrid promoter show, for the first time, that: (i) the HO promoter is modular since mother cell specificity can be replaced by galactose dependence without compromising cell cycle control or a/alpha repression; (ii) transcription of HO is indeed the major rate-limiting event for switching which is absent in daughter cells; (iii) SWI1,2,3, 4,6,7,8.9 and 10 are unlikely to be involved in mother cell specificity but SW15 probably is.

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Wiley Icon for PubMed Central
Loading ...
Support Center