See wiki, epigenetics, for a short article on a big subject. Somaclonal variation just means a change that happens in a clone of somatic cells; that is not by recombination of genes in the usual way that happens is germ cells, which make eggs or sperm. It can caused by be many things. Some are major disruptions in chromosomes, like translocations. Others are small, like hormonally induced methylation of some particular DNA sequence that results in somehow giving a detectabley different phenotype to the plant. In potatoes it was noticed as different shapes of leaves, texture of the skin in Russett Burbank. Whatever you can see that matters would be scored that way, as somaclonal if you grew a clone from somatic cells.
With roses the stress effect of cutting out the axillary bud, knocking of the main shoot etc could stimulate hormones to make cells grow abnormally. While doing so they might give rise to mutants. The growth of cell layers not normally active might also happen. It would be a somaclonal variation, that is, not from a cross-pollination. That’s what a sport is, now that I think of it. Most somaclonal variation is observed in tissue culture where you do strange things to the cells. Putting 2,4-D on a bud might have a similar effect. So could too much gibberellin, or cytokinin.
These treatments might also result in epigenetic effects. That is, they don’t change the fundamental sequence of any DNA (the order of the 4 bases that make it up), but they still give a different phenotype. Methylation of some bases in DNA makes them not recognizable by certain regulatory factors. Some modifications of proteins called histones can have a similar effect, because histones bind DNA and also regulatory proteins. This is all very complicated and poorly understood in general. It is very well understood in some certain specific cases. We generalize from these to the whole genomes, not really knowing quite what we are talking about.
In animals there is a concept called imprinting, where certain genes from either male or female gametes are turned on or turned off selectively. The wiki article mentions a couple of syndromes caused this way. They are real and well understood. There is also X-chromosome inactivation in female mammals, to keep the proper balance in X-X compared to X-Y.
This is directly related to the notion that some traits in roses are predominantly gotten from staminal or pistillary parent. It is a kind of maternal or paternal inheritance that does not depend on the plastids and mitochondria. I don’t know of much good evidence for it, but some people feel that it happens.
Linkage disequilibrium, which I think I wrote about in the RHA newsletter a few months ago, could in part be epigentic in basis. Some genes on different chromosomes need to go together to make some things happen, or other things not happen. So certain combinations of chromosomes may make a non-viable gamete. Thus you will never find offspring that break he linkage of some traits, even if the genes encoding them are on separate chromosomes. That means that any genes close by these will usually get carried along and will seem to be linked to each other, though they are also on different chromosomes.
The epigenetic and linkage disequilibrium effects may be especially severe in wide crosses like hulthemias, or some other species crossed to common garden roses.
I realize this is pretty far from axillary buds, but its a big part of the breeding process.
). I removed the leaf and saw these two buds. This wasn’t a consistent characteristic. On some leaves there was only one present and on others two like this were evident. So I’m wondering whether one of these buds is actually a secondary axillary bud or just what the authors of this paper call an adventitious bud.