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INTRODUCTION JUNE YELLOWS IS a progressive, deleterious variegation of the cultivated strawberry. Repeated attempts have failed to transmit the disease, by possible insect vectors or by grafting, to unaffected plants. Heritability was first demonstrated by Clark (1930) and later by other workers, but early attempts at genetic analysis were inconclusive. Darlington and Mather (1949) suggested that the disease might be caused by a mutant plasmagene and the subsequent experimental results of Williams (i) and McWhirter (i) were consistent with this view. Genetical investigation of June Yellows at this Institute was stimulated by the rapid decline of the variety Auchincruive Climax (hereinafter referred to as Climax), and the widespread occurrence of the disease in seedlings and advanced selections bred here. 2. SYMPTOMS Symptoms appear in Scotland with the start of spring growth, reach a peak in May, and fade and disappear in late spring or early summer. They may reappear in autumn, but never at the earlier frequency or intensity. Symptoms were described by Williams and by others. Leaves expanding in early spring vary from a nearly uniform pale yellow colour to a light mottle of green and yellow. Successively later unfolding leaves have a more conspicuous mottle, with an increase in chlorophyll colour in some cells. These stages are seen in plate Ia. Chlorophyll continues to increase as leaves age and the mottling may disappear. Reid (1956) reported that the development of green colour in leaves was accelerated by growing plants in a warm greenhouse. McWhirter noted that symptom distribution reflected an influence of cell lineage. Permanent white streaks, often coupled with leaf distortion, appear spasmodically in Climax, Cambridge

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S U M M A R YCrude extracts from cotyledons of 2-day-old seedlings were separated by electrophoresis on polyacrylamide gels and stained for acid phosphatase. At least 22 bands were recognised, distributed over seven zones. Analysis of zone 1 allowed estimation of sib frequencies in 12 out of 19 hybrid cultivars. By applying either seedling zone 1 or acp-2 seed acid phosphatase analysis, sib estimates could be made in 15 of these hybrids. It is suggested that this technique offers a practical and rapid means of estimating sib frequencies in commercial seed stocks.

SUMMARY Extracts of seeds of Brassica oleracea L. cultivars were separated by electrophoresis on polyacrylamide gels and stained for 14 enzymes to investigate the possibility of utilising isoenzyme variation to determine sib frequencies in hybrid cultivars. Acid phosphatase (EC 3.1.3.2), cr‐amylase (3.2.1.1), carboxylesterase (3.1.1.1), β‐galactosidase (3.2.1.23), β‐glucosidase (3.2.1.21), leucine aminopeptidase (3.4.11.1) and peroxidase (1.11.1.7) reactions gave discrete bands. Three broad zones of acid phosphatase activity occurred and control of banding patterns in the intermediate zone by a series of co‐dominant alleles was confirmed. The locus is designated acp‐1. Sib frequencies could be estimated in eight of 21 F1, cultivars examined, since their parent lines were homozygous for different acp‐1 alleles. This method of estimation has several advantages and offers a practical alternative to current methods. Routine determination of sib frequencies by using any of the other enzymes investigated is impractical.