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The full model comprises the entities shown below plus the hypotheses postulated for them. 2-6 GENOT-1 GENOT-2 α1 GENOTYPE-OF-PROG-1 ♣♣♣ ❍ ❍ COMBINATOR ✟ ✟ αs GENOTYPE-OF-PROG-s DETERMINER ❍ ✟ ❍ ✟ ❍✟ ❍✟ r PHENOTYPE-OF-PROG-1 PHENOT-1 ♣♣♣ ❍ ❍ 1 DISTRIBUTOR ✟ ✟ ✻ PHENOT-2 rk PHENOTYPE-OF-PROG-k ✟❍ ✟❍ ✟ ❍ ✟ ❍ ✒ APPEARANCE PROGENY-1 PARENT-1 ♣ ❍ ❍ MATOR ♣♣ ✟ ✟ PROGENY-k PARENT-2 On the right hand side we cannot draw the arrows for DETERMINER and APPEARANCE in the same orderly way as on the left hand side because the mappings need no longer be one-one.

Present thinking is, however, that this process is under genetic control, and it remains a major programme that the biochemistry of COMBINATOR be investigated. It should be stressed that use of the techniques of relative frequency measurement, as per transmission genetics, do not satisfy this programme. Even if the loci and characters are described in biochemical terms this is not sufficient to provide a molecular genetical version of COMBINATOR, although this would be necessary. It would be too simple to say that genotypes are purely theoretical constructs.

Such a model we call a combination kinematics. As the label indicates, the present task is just to describe how the chromosomes change their configurations in time, and not to explain why they do so. The latter task would afford a truly 2 See (Morgan and Bridges, 1916) and (Dobzhansky, 1932). 50 dynamical model in which the ‘forces’ responsible for the changes are made explicit. In the present chapter we want to refine the previous model to include such a combination kinematics. Since we want the refined model to be as general as possible (to cover as much of genetics as possible) we do not bring the full cyto-chemical machinery into play.

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A histone H3K36 chromatin switch coordinates DNA double-strand break repair pathway choice


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