secondary axillary buds in roses

Back sometime in 2007 Larry Davis put this link up in a discussion about using sports as breeding parents (see link)

I was wondering whether roses have these secondary axillary buds? This is a photo I took tonight of a Climbing Iceberg stem (coincidental that it is itself a sport… I just chose a stem from the vase of roses I picked for my wife the other day… shhh don’t tell ok :wink: ). 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.

I’m thinking that if it is a secondary axillary bud then it would be interesting to experiment with a sport such as Burgundy Iceberg to see first whether the mutation seems to be inheritable without such intervention and secondly whether by removing the terminal and primary axillary buds and pollinating flowers from the resulting secondary axillary buds you might be able to force some degree of inheritance of the mutated characteristic. Today I did a Iceberg x Burgundy Iceberg to see what happens.


The secondary axillary buds are common on roses. How much they are expressed is very variable.

(With Rose Rosette Disease, these axillaries break and more form, and more and more. The most I have counted at one RRD sick bush (Snowdrift, up in Canada) had eleven axillary buds at a single leaf axil.)

Often we can see double breaks (maybe,as many as three,) on totally healthy roses, sometimes below where a stem is cut way back on a healty cane. Two or even three canes can emerge from such a push to keep on growing by that rose cane.

Thanks Ann. How would distinguish between these secondary axillary buds and adventitious buds? This stem (above) came from just below a flower and the plant appears to be quite healthy and vigorous. I suspected RMV at one stage but now I am not sure.

The word adventitious as I’ve heard it generally refers to roots.And specifically roots that develop from up on a stem and grow (obviously) downward.

The link below to an Oregon State university site separates axilary buds and adventitious buds rather well and distinctively.

The use of adventitious tissue for cellular propagation is something I will try to watch for as I slog through scietific papers.

Hope the link helps.


I think it was claimed I started all this though I don’t recall. An example of secondary axillary buds is the following. T-Bud a pear or apple onto a root stock. Kill the obvious bud by some injury. Come spring, cut the top off the stock anyway. A good % of time two little tiny buds will form and produce shoots on either side of where the dead bud was. My thinking is that these were potential buds in the leaf axils of the bud that was killed. They probably arose from meristem tissue in these locations. But as described in the article posted, they could come from different layers.

If you take a cutting to grow a rootstock and cut out all the obvious buds while rooting it, or later while grafting it, you may get shoots anyway, if the budded plant fails. These may be adventitious buds, or secondaries from an axil not cleanly cut.

While detectable sports depend on color or growth habit for detection, there may be many sports that go unnoticed, or get discarded in propagation. It seems that the most sporty roses have been those like Ophelia, or Peace, that were grown in millions, propagated rapidly and used under hothouse conditions as greenhouse roses. The rapid growth, use of every available bud in production, and large numbers generated in a literal or figurative hothouse probably increased the sportiness. In a plain red, white or yellow you’d have a hard time detecting sports unless they were extreme, like a climber out of a shrub, or a switch from red to white or vice versa.

Somaclonal variation is something well studied in plants grown in tissue culture where the cell division is very rapid, under somewhat stressful conditions. This was used to practical advantage with potatoes over 30 years ago. This is like adventitious buds in many ways. My prediction is that you will find far fewer sports with own-root roses like the minis, even those grown in the millions, compared to budded roses.

Sorry Larry… my mistake it was Jim Turner. Don’t know why I put your name down as the source. Sorry about that. This is the thread to which I was referring (see link).

I’m not particularly interested in making new sports, but sometimes I look at existing sports and think I’d like to use them in a cross but don’t because there is a good chance they will just breed as the original plant anyway (like, hypothetically, ‘Burgundy Iceberg’ breeding as a white instead of a burgundy). I know there are sports that do pass on the sported genes (and I wonder, after readng this, whether the flowers from which pollinations were made actually did come from secondary axillary buds or whether budding material came from secondary axillary growth), but there are a lot that don’t too. This article seems to suggest that if the primary axillary bud and the terminal bud is removed to trigger the growth of the secondary axillary bud then they could achive some level of ‘reorganisation’ of the sported genes from L1 or L3 into L2 where it could influence the development of gametes because the fidelity of secondary axillary growth was much lower than that of the primary and terminal bud growth. This is an section from the article:

“The eradication of terminal and primary axillary buds led to the outgrowth of secondary axillary buds, in which the fidelity of apical cell layer organization was highly compromised. It was demonstrated that seed could arise from apical cell layers that are genetically distinct and developmentally isolated from adjacent cell layers in certain types of genetic mosaics. The end result was the recovery of seed progeny possessing genes that were developmentally isolated in the cell layers of the shoot meristem that would not normally generate gametes.”

I was just wondering whether it might be possible to ‘encourage’ a sported variety to make gametes that possessed the mutated DNA by first using a variety that is a known sport and then removing the terminal bud allowing the primary axillary bud to grow and then removing the primary (and possibly lower buds) to encourage secondary axillary buds to grow that might in turn encourage the plant to reorganise the mutated DNA into the L2 layer where it might then be inheritable and useful to hybridisers.


It would be worth trying if you have a sport that is something special, and that doesn’t pass the special characteristic to its offspring. The odds of success may not be high, but if you are bothered by long odds, you shouldn’t be breeding roses.

Thanks, Simon, I just thought I was getting absent-minded but I usually recall having read something, if not some of the things I have written. I guess my experience with sports is limited. CLimbing Crimson Glory OP always gave me all climbers, and not remontant. New Dawn x repeat bloomers gives seedlings that bloom first year, though repeat bloom is sometimes stingy.

Perhaps some sports are epi-genetic. Now that we’re beginning to understand how microRNAs and such work, and how methylation of DNA can turn things on and off, it is easy to imagine. Some of the somaclonal variation that I mentioned is epigenetic. For potatoes, or budding roses, that’s fine. For the breeder its frustrating not to be able to carry the trait through a sexual generation. Some genes can be turned off for generations if the germ line is affected. Others are reset every time.

This problem is not trivial. I think it explains why you don’t get darker and darker red with every red gene you add. for instance. That’s what they found with purple petunias- they didn’t get darker, but lighter due to RNA interference with expression of the excess copies.

Griffith Buck noted the challenge in breeding Carefree Beauty. Too many pales and whites even when multiple pinks were combined. I see the same with C.B. If it had 2 red genes out of 4 possible, some of its selfs ought to get all 4 and be red. But they’re not. They’re just like C.B. So there is some interference, whether in not permitting truly random assortment of chromosomes, or a modulation of expression of the red genes. I also noted in this month’s newsletter, that a cross of C.B. x General Jac never gave a seedling as dark as General Jac. Etc.

It could be possible that other genetics are interfering.


I think Carefree Beauty might be able to produce some o.p. red seedings. I have one which can be viewed at It is definitely not anything pretty to look at, but it did have a nice, red color (Much deeper in real life).



Thanks Andy for the photo. That is a reasonable red. My point was that I don’t get a quarter, or even 1/8 decent reds. I never kept records on CB selfs, just looked at them. I did find some records on the following. In all these CB was the mother. With:

Gold Masterpiece, 11 pink, 10 pale, 1 yellow.

Black Jade (dard red mini), 2 pink, 2 red.

Mirandy, 9 pink, 1 red.

Crimson glory, 40 pink, 2 dark pink, 0 red.

Another attempt with Cr. Gl., 12 pink, 1 white, 1 red.

Gen Jac gave a few dark pink, no true red. An example is shown in the latest newsletter

Sorry for the late reply… I have been away for a few days for some much needed R&R.

Just so I understand… by epi-genetic do you mean dermal layer mutations? I guess that’s what sparked my interest in the article Jim posted. It seems to suggest that by forcing a less accurate form of growth to occur that genes that would normally be isolated from the germline could be shuffled across into it and therefore become inheritable.

Regarding the impact of genes that get switched on and off… I am less sure what you mean. I know about the Operon Theory and I know of cascading genes and homeotic genes and how homeotic genes initiate gene cascades etc but I understand this in the context of limb formation in animals… so I’m assuming you are referring to something different in the context of these non-inheritable somaclonal mutations.

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.

OK… so what you are saying is that the phenotype of the cells in the different layers of the plant tissue may be different but the genotype may be the same. I think the article makes things confusing for me because it uses variegation as the reference feature and my understanding is that this is chimeric (i.e. different genotypes). So, if I understand the significance of what you are saying, under normal circumstances when a sport occurs it can be due to the existing DNA being ‘interpretted’ in a slightly different way resulting in somaclonal variation which may be heritable in the lifetime of the individual (i.e. through cell division) but not necessarily from one generation to the next. So under what circustances can epigentic effects result in changes to the germ line in plants so that they are then heritable from one generation to the next? Does this bring us back to the three layers of organisation of plant tissue described in the article and the isolation of genetic material between there layers? So if these epigenetic changes occured in the layer from which gametes are derived then they may be heritable and if they occured in the other two layers then the only way to perpetuate them is by vegetative propagation?

When I was at uni one of our biochem labs was to investigate the effect of various concentrations of auxins on the growth of axillary buds in pea plants. We pinched out the terminal bud to trigger the growth of the axillary buds and added various strength gibberelic acid to them. The effect on internode length was significant but not inheritable because self-pollinated seedlings from the flowers on longer manipulated stems showed no internodal variation from the parent line. Hmmmm… I wonder if we had of tipped these longer stems treated with gibberelic acid and then rubbed off the resulting primary axillary buds to allow the secondary axillary buds to grow then self pollinated flowers on these secondary growths whether we might see some kind of evolutionary change… so long ago now… wow… that’s Lamarckish isn’t it!

I guess there is also the question, what if the sport has occured through more traditional mutagenic processes such as point shifting, frame shifting, insertions, deletions etc? It still may not be heritable would it?

I think the only way to know if the germ cells got the sport is through breeding. Of course it can be traditional mutation, most likely in some regulatory sequence, like a place on the DNA where some factor is supposed to bind, to control the level of expression of some gene, maybe, for instance, the rate limiting step in pigment production. And maybe the pigment is made in response to sunlight or temperature or stress. In cabbages, in fact brassicas in general, lots of stresses stimulate anthocyanin production. The pigment which happens to be red, protects against sunburn (no joke) by absorbing the UV. The photoresponsive roses are probably of this kind. And some make more color in hot weather. For instance I had pink flowers on Harrison’s yellow when late-breaking buds bloomed in June- a month late and quite hot here. And of course tea roses often have complex shading as a function of age and temperature and light.

The genes that determine pigmentation pattern are easy to see changing over time in a single flower, or through various sports. That’s how most garden flowers were selected from their wild progenitors. If any are epigenetic, I don’t know.

Yes, the epigenetics stuff is rather Lamarckian. There have been some articles on this in New Scientist, Science, Nature, over the past few years commenting on that. But remember that Darwin was a Lamarckian for many years. He didn’t know a thing about genetics as we understand it. And dog breeders still believe in bloodlines, and polyspermy, so if a female mates with a mongrel, her offspring later can not be registered as thoroughbred.

Rose breeding is still an empirical science.

Thankyou for your responses Larry. I have thoroughly enjoyed it. I don’t get much of a chance to use my training anymore (yr8 science students tend to be interested in other things…). It feels really good to be able to apply it to my hobbies.

Thanks again.

Simon, If you work with yr8, by all means try Wisconsin Fastplants. You can look up their website and read details. It is a great way to learn basic genetics, and also plant physiology. We did some work on gravity response, UV sensitivity etc with kids from yr5 on up. And with their teachers.

Getting seeds to your continent may be an issue, but Paul Williams, the inventor of the plants, is a retired cabbage breeder and would know how to do it legally.

We had fast-plants here too… they were brassica of some description from memory. It’s been a while since I looked at them because at the time they were mainly just to demonstrate the life cycle of plants and didn’t have genetic applcations (that year 7-10 students would understand anyway)… this was about 10-12 years ago now and it sounds like they have come a long way since then. I love doing geotropic experiments with the kids. I put a raddish seed on an agar plate and then sit it on a lump of plasticine so the kids can turn the seeds once a day creating step-shaped root development…