John Robert Stanley Fincham. 11 August 1926 — 9 February 2005

Professor John Fincham was one of the UK's leading geneticists, with a remarkably broad knowledge of the subject across all the biological kingdoms. He became an international leader through being at the forefront of microbial genetics as some of the founding principles of the relationships between gene structure, activity and enzyme functions were being uncovered. He spearheaded discoveries from the one gene–one enzyme concept, through genetic complementation, protein structure and recombination. Much of his experimental microbial research centred on the genetic and enzyme variants of glutamate dehydrogenase in the fungus Neurospora . He also brought his outstanding mind and comprehensive interest in genetics to the then obscure features of unstable genes and transposable elements in plants. His standing was recognized by holding prestigious chairs in Leeds, Edinburgh and Cambridge universities. He was a talented writer, producing several textbooks and especially the leading text Fungal genetics . He was also a practitioner and lover of sports and in his early career was politically active. His successes in life made him an extraordinarily talented man who achieved much as a leader in genetics in the UK and internationally.

A Modified Autonomous En Transposon in Maize (Zea mays L.) Elicits a Differential Response of Reporter Alleles

Transposable elements in maize are composed of a defined molecular structure that includes coding sequences, determiners of functionality and ordered terminal motifs that provide binding sites for transposase proteins. Alterations in these components change the phenotypic expression of unstable genes with transposon inserts. The molecular basis for the altered timing and frequency of transposition as determined by the size and number of spots on kernels or stripes on leaves has generally been described for defective inserts in genes. Most differential patterns can be ascribed to alterations in the terminal motifs of the reporter allele structure that supplies a substrate (terminal inverted repeat motifs) for transposase activity. For autonomously functioning alleles, the explanations for changes in phenotype are not so clear. In this report, an En-related element identified as F-En is described that shares with En the recognition of a specific defective element c1(mr)888104 but differs from En in that this F-En element does not recognize the canonical c1(mr) elements that are recognized by En. Evidence is provided suggesting that F-En does not recognize other En/Spm-related defective elements, some of whose sequences are known. This modified En arose from a c1-m autonomously mutating En allele.

Unstable genotypes

Unstable genotypes are normally recognized in cultivated plants by the appearance of coloured spots or flecking which are easily seen and scarcely affected by the environment. Unstable genes giving variation in characters such as plant mass, height, yield and earliness are unlikely to be recognized because normally it would be virtually impossible to distinguish such variation from environmental variation and other genetic variation normally ascribed to segregating genes, without deliberate search and detailed analysis. Continuous variation may contain a host of instabilities, or their more stable products, which could have had their origins in the many normal processes of differentiation. It is not known how easily heritable changes can be induced by the environment in plant species in general, but in flax and Nicotiana rustica environmentally induced changes giving large relatively stable differences in plant mass, height and flowering time provide a means of studying the behaviour of unstable genotypes affecting these characters. Crosses between environmentally induced flax types and varieties show that the phenotypic differences are not essentially any different from, and could be dispersed unnoticed among, the rest of the genetic and environmental variation. They also show additivity, dominance and gene interaction, and they can be the cause of asymmetric response to selection and inbreeding depression.