Genetic aspects of yeast flocculation: in particular, the role of FLO genes in the flocculation of Saccharomyces cerevisiae

Abstract

Lectin-mediated flocculation has been shown in a number of yeast species and genera. The genetics of flocculation have lagged behind other areas of study and to date, have only been studied in the mannose-sensitive form of flocculation (Flol phenotype) in Saccharomyces cerevisiae. Some 40 years ago, flocculation was shown to be an inheritable characteristic of certain yeast strains. This demonstrated that flocculation was not a purely colloidal or chemical phenomenon. A number of dominant FLO genes were later discovered. Yeasts containing FLO genes after genetic crossing, were found to flocculate. FLO1, FLO2 and FLO4 were allelic and currently FLO1 (chromosome I), FLO5 (chromosome I) and FLO8 (chromosome VIII) are recognised. Flocculation may be suppressed by genes fsu1 and fsu2. Non-flocculent strains have been shown to flocculate following mutation at the TUPI (chromosome III) or CYC8 (chromosome II) loci. Other mutations, abs, wal, FH4C, sfl1, cka2, also cause flocculation, as does expression of human HA-ras p21 or viral HTLV-1 tax, or over-expression of yeast CHS2. In view of the similarity in flocculation caused by FLO genes and tup1 or cyc8, it has been suggested that most, possibly all S. cerevisiae strains contain lectin genes which are expressed following regulatory mutation. It is therefore possible that FLO genes are regulatory rather than structural lectin genes.