Unexpected repeat blooming

A couple years ago I pollinated the species rose R. palustris with pollen from the hybrid rugosa ‘Apart.’ I got two seedlings from it, one of which survived infancy and went on to grow faster than anything else in my garden and in the second year of its life, produced a nice crop of semi-double blooms early in the summer like I expected it to but this year it has done something rather unexpected – I’ve moved away for college, and haven’t gotten a place for my roses down here yet, so they are all under the care of my mother and little sister. And talking to them today, my little sister mentioned as if it wouldn’t be of any interest at all that it was blooming again, just a few blossoms here and there. My jaw dropped. It is repeating its bloom! How is that possible? In a cross between a once bloomer and a repeat bloomer, how can we get a repeater? Especially since the mother is a pure species rose, no chance of any hidden repeat blooming genes or anything. I of course start wondering if it isn’t a species at all, but some sort of hybrid, but there are no signs of it. I have never detected any irregularities of what one would expect from the species in it. And indeed, I have grown OP seedlings from the same parent to plant in a wild rose hedge in a wild part of the garden, and none of them have shown any signs of unexpected parentage.

Any ideas how this recessive repeat blooming gene from the father could show up despite the dominate once blooming gene from the mother?


I am getting some “repeat” blooming from a number of roses this year that did not exhibit that characteristic in the past. I wonder if these are “late” first blooms caused by the cold wet long spring this year.

R. foliolosa X R. rugosa produced ‘Anne Andt’ and ‘Basye’s Purple’, both of which are fully remontant. There is more to working with non-remontant species than is immediately apparent. Personally, I have evidence to believe that there are different genes for remontancy in differenct sections of the genus Rosa. I can elucidate if you want to know why I think this.


Paul, I’d be very interested to hear about your evidence for different remontancy genes.

I second Jim’s motion – please elucidate Paul!

I second Paul about things being a lot more complicated than dominant: once blooming / recessive:recurent.

I.e. you can get once blooming from crosses involving only remontants.


Pierre is right, you can get once-bloomers from crosses involving two fully remontant parents. Case in point: Crosses using ‘Out of Yesteryear’ pollen on any other remontant modern rose gives about 30% non-remontant offspring. I speak from personal experience, having grown hundreds of seedlings from various crosses using this as a pollen parent. And yet ‘Out of Yesteryear’ is extremely reliable with repeat bloom. Every generation of R. bracteata hybrids appears to give a percentage of non-repeaters.

Another case: I have worked for several years using the Portland Damask ‘Marbree’ as a parent, crossing it with Miniatures and other modern remontants. Over 80% of the progeny are once-bloomers, no matter how remontant the other parent. ‘Marbree’ itself is a reliable repeater, blooming with three to four flushes a year.

Now think of this: consider the origin of the first Noisettes. Genetic testing has illustrated that the first Noisettes are crosses of R. moschata X ‘Old Blush’. Even though R. moschata blooms late in the season, often flowering till frosts, it is still a once-bloomer, and yet when crossing it with ‘Old Blush’ it resulted in the fully remontant Noisettes. This suggests that there are different genes that control remontancy, and unless you match the right genes, you can end up with once-bloomers. Inversely, sometimes once-bloomers crossed with remontants can give some remontants. This flies in the face of the straightforward Mendelian basics of inheritance, suggesting that there are mechanisms invloved that we do not understand. Could cytoplasmic DNA have something to do with this too? Who knows.


Hi Paul, just a note to say the OP seedlings of ‘Precious Dream’, (‘Orangeade’ x ‘Out of Yesteryear’), that I sowed for a lark late last year all appear to be fully remontant. This season I’ve had no hips form on ‘Precious Dream’. I had several last year. Apparently the weather has been less conducive to hip formation this season. Thanks, Robert

I do not remember the details, but Karl King (at least I think it was him) once discussed this trait (repeat blooming).

The following is what I think he said: rather than thinking of only a gene to cause repeat flowering, perhaps we should be thinking of having or not having genes to turn off flowering under certain conditions.

------End of what I remember (or think that I remember about what Karl said).---------

For example, there is a “rule” to remove spent blooms as that often encourages repeat flowering. Also, the amount of light affects the ability to flower. Same is said for the ratio of nutrients. It would appear that flowering is controlled by a complex set of conditions.

I will see if I can find Karl’s original communication.

A few other cases along these lines…

I have a multiflora X rugosa that has repeated faithfully every late summer for about 5 years. The multiflora seed parent probably has some other ancestry in it, since it is double-flowered (with 20 - 30 petals). I had assumed that it carried a hidden repeat-flowering gene from some modern rose. This might not necessarily be the case. I’ve read that some other rugosa X synstylae hybrids, like X kordesii and X paulii, will produce some fall blooms.

Another case in point, I read that rugosa X arkansana (both of which repeat), gave all once-bloomers.

I have rugosa X carolina (both of which repeat). So far, it looks like this one will follow the path of the previous hybrid and give all once-bloomers.

I have ‘Fragrant Cloud’ X carolina (both of which repeat). These are definitely not repeat bloomers, since they’ve gotten quite large and haven’t bloomed even once yet.

So, I would go along with the idea that there are multiple genes and different types of repeat…not a simple dominant vs. recessive situation.

Just to add food for thought, I have a friend that crossed ‘Champney’s Pink Cluster’ with ‘Katherine Zeimet’. While one would expect repeat flowering, this seedling didn’t produce a single flower for the first seven years. Now it repeats regularly and is truly a lovely thing at that.

I finally cut down a huge seedling of ‘Crepuscule’ this year that had never flowered after four seasons. Is there a genetic trigger that takes over at maturity to induce flowering as well? I don’t have the space to find out. It’s certainly is frustrating to wait and wonder. I guess one has to weigh the value of the cross if one isn’t to save everything. Thanks, Robert

I found the article that I was thinking of, and it was not written by Karl King, it was written by Ryck Birch.

The following is a summary (the article is 4 pages):

There are two sources of remontancy in our hybrid roses. One line comes from the Autumn Damasks/Damask Perpetuals [DPs]. The other from the Chinese roses. Both of these lines started being actively developed at roughly the same time [the DPs got a head start; some work was being done with them–not much–before the Chinese roses hit Europe].

The Hybrid Perpetuals [HPs], which arose out of the combination of the Chinese and European rose stocks, were remontant, that is, they rebloomed, but were not continuous bloomers in the sense that the Tea roses were or our modern Hybrid Teas [HTs], Floribundas [Fs], et al., are. In fact, they show a considerable range of ability in rebloom: from the scant flower in the fall to generally consistent and reliable cycles of bloom (like our modem roses).

It is possible that we are looking at the competition of 2 sets of genes: 1) those for blooming, and 2) those that shut off blooming. Further, let us assume that each of these capacities follows quadrivalent inheritance patterns.

In nature, a plant in the temperate world does not want to keep flowering on into winter. It blooms and then ripens its fruit. This takes time and energy–typically more than what is required to make additional vegetative growth. The plant’s general growth cycle includes the sequence of bud-sprouting, growth, flowering, and ripening of seed. Under normal circumstances, the plant undergoes a response to the signal that it’s the right time to grow and flower. The flowering genes are switched on, initiate flowers and then are switched off.

Remontancy, in general, would then be a malfunctioning in one, the other, or both of these growth regulating mechanisms. Such malfunctions would center on 1) the gene(s) for flowering not shutting down when finished with its(/their) activity in response to the shut down signal: “Spring is over, time to stop flowering”, or, 2) on the inability of that(/those) stop growing signal gene(s) to function.

I have “watered down” the scientific level of his comments considerably. In doing so, I hope that I have not lost his intended meaning.

He does discuss the rugosa behavior (which would apply to the question in this thread of whether there are two types of remontancy genes). The following is a quote:

“Generally speaking, I would expect that cold climate adapted remontancy would take the form of the lack of rebloom suppression while warm climate adapted remontancy would be based on lack of flowering genes being shut off. I am particularly thinking of R. rugosa in this regard. Fast seed ripening presumably allowed such a mutation–no rebloom suppression–to survive and multiply. I would also imagine that the Chinese roses may have been more weakly selected for rebloom suppression given their mild climate. (This would have bearing on the problematic issue of getting these roses to go dormant those of us in the North.)”

Thanks Henry for the summary (although I’d love to read the full article). I had thought about the (at least) two sources of remontancy in modern roses (i.e. Damask Perpetuals and Teas).

I also wanted to mention the concept of “polygenes”, or another way to call them would be “modifier genes”, so the possibility is that a rose could be genetically remontant, but the polygenes could affect the expression of that gene. Some would appear to be non-remontant, others might bloom themselves to death and most would fall somewhere in between (which would help explain the variance in blooming between different roses). The ones that appear to be once blooming, might, given appropriate conditions. bloom more than once on occasion.


Damasks Perpetuals or Teas?

Rather: All the Damasks (expressed or not), R.Chinensis, R.Fedtschenkoana, R.Rugosa, some Multifloras, R.Arkansana, R.Moschata…These are the ones I know, there are many others, without doubt, wich carry the potential for reblooming.

The idea “reblooming came from R.Chinensis” may be true on anb historical point of view, but from a botanical one it’s an old nail.

Best wishes,


Thanks Henry I do have more than a good hypothesis about this repeat/no repeat blooming genetical problem.

For years I was questioned by the not at all rare reblooming among once bloomer hybrid seedlings from once blooming species. And the suposed once blooming dominance…

Only answer I found to these facts was that these


I like that hypothesis. It makes good sense, that once-blooming (regulated blooming) genes would develop to adapt blooming to its best possible timing. It also makes sense, that the once-blooming genes could respond to different cues in different species.

I think these ideas are more in tune with the observations we’ve all made (as rose hybridizers), than a simple dominant/recessive hypothesis.


I too find Pierre’s comments very interesting, and somewhere “up to date”.

I believe there are many species that have the ability to rebloom, but hidden. A bit like species who grow on poor soil, and that give double flowers whenever planted in a garden soil.

Another observation I made is about the “not very remontant” roses, I.e. some Damasks Perpetals, some Hybrid Perpetuals.

These roses, here in my cool climate and very rich, heavy soil, can rebloom even better than Hybrid Teas, provided they are at least five years old. This means continuous flowering from June to October!

Examples: Duchesse de Portland, Mme Boll, Eug

Pierre has an interesting insight, and one that makes sence.

The idea that repeat blooming is the result of a befective gene to shut down or prevent blooming would acount for repeating species croses (rugosa X carolina) not reblooming. It could be that the deficiency in the mechanism to halt blooming is repaired in such croses.

It would be intresting to know what chemical signals are involved in the expression or supression of reblooming, I wounder:

If there is achemical signal to halt blooming, could a systemic spray be developed to block that signal?

If the opposite is true and there is a repeat blooming gene, could that chemical signal be identified and incorperated into a systemic spray to induce repeating in non repeaters?

Wish I was qualified to look into that one.

There’s the 1999 paper describing giberellic acid as signal for repeat bloom. There are many slightly different forms in plants making studying this tricky. However, there is decreased GA in the spring right at or after bud break in one time blooming roses and at this point the meristem converts to floral. So, cold (vernalization) seems to reduce GA concentration (opposite of what we typically think of for seeds). The authors sprayed GA on R. wich. and Fel. et Pep. (old rambler) and it’s repeat flowering sport (‘Little White Pet’) early in the season and found it hindered / stopped flower development in the first two roses, but for LWP it didn’t. Their idea was that the gene for GA was so defective in LWP and producing GA at such low levels that the plant couldn’t absorb enough to hinder flowering. So, this gene that needs to be in a homozygous recessive form for repeat flowering probably is just a defective GA gene and when homozygous recessive the plant cannot produce enough of a viable product to hinder flowering. Perhaps across roses species and different cultivars there are slightly different versions of the mutated gene and sometimes there may be some complementation or other things that happen for the odd outcomes for repeat flowering we see in some crosses.

I tried AMO1619 (off the top of my head I think this is the number), a GA binding chemical. on some young plants of a one time blooming rose to see if it would allow it to flower without vernalization. It didn’t flower. Perhaps the opposite is true here to LWP in that there is so much GA in the plant that spraying some GA binding chemical on the plant cannot bind enough within the plant to get below the flowering threshold.

There is definately a lot more work that can be done in this line of work. I summarized this paper in an RHA article and offered some of my ideas where this work may go a couple years ago.