Rugosa remontancy???

Quick question… is rugosa remontancy the same kind (genetically speaking) as that found in other modern roses? In my 2009 rugosa x modern seedlings there is no hint of flowers yet (though I understand this is normal and that remonatncy can develop as they mature over the next few years), when other 2009 modern rose seedlings have begun flowering already… so was wondering whether there was any different types of remontancy (apart from juvenile onset, and mature onset etc).

Rugosa seedlings, for me, normally take about three years to start flowering- but once they do, they flower with remontancy.

Rugosa seedlings have delayed first flowering. With a long first growing season one will get a small percent of first year flowering. This earlier flowering of rugosa is little or not heritable in my experience.

Rugosa hybrids as a rule are not earlier flowering than the species.

Many build quite large plants before flowering.

Persisting beyond F1 along fertile progenies one can effectively breed out (or break down?) the rugosa delayed flowering.

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Hi Pierre

how long does it take to breed out the rugosa delayed flowering?

Ok… I’m aware that rugosa usually has a delayed onset of remontancy… but… is there different kinds of remontancy or is it something else that is affecting the expression of its remontancy, which is the same as is found in other modern roses… when you breed it out are you replacing the rugosa remonatncy habits with modern rose remontancy genes or are you removing the genes that delay the onset of remontancy?

when you breed it out are you replacing the rugosa remonatncy habits with modern rose remontancy genes or are you removing the genes that delay the onset of remontancy?

Rather difficult to know. As I do not backcross to moderns the first hypothesis (replacing the rugosa remonatncy habits with modern rose remontancy genes) is unlikely. As for removing the genes that delay the onset of remontancy…it is done somehow.

My interpretation of what is happening is that delaying genes expression is hindered by a different from the original one, modified, non cooperative genetical environment.

This is IMO how one can get F1 recurent seedlings from a non recurent species.

For me this absent or delayed recurence break down occured often enough either in some F2 or better in some F1 x a different species background F1.

I.e. years ago I got an early low first blooming seedling from the foliolosa x rugosa cross F2.

And this year from crossing a complex recurent hybrid involving mainly bracteata, foliolosa and rugosa on which laevigata pollen was applied I got out of a few a recurent seedling. It is flowering to now from a june beginning.

Same break down as for non recurence is observed i.e. for desease resistance, scent or spines.

< is there different kinds of remontancy…?

Most think so. As you see I do not.

However it does not matter as long as we have fun playing with roses.

It would be interesting to cross pure rugosa with the more pure chinas to see how the seedlings play out. I do know that there are a few hybrids like this out already, but I am interested in the story all of the seedlings in total show.

2yr is the usual time it takes me to find reblooming in Rugosa x Chinas. Perhaps it is the shortness season of my northern garden that may push them faster. I can’t understand if I am doing anything unique. I could be like Suzanne which only reblooms in northern gardens?

I had a thought the other day about remontancy, after having read an article posted by Henry Kuska recently. The article described gibberellins as being a key factor in remontancy. If gibberellins are the main factor… then shouldn’t it be possible to select for either of the following two variables?

  1. more or less production of gibberellins

  2. more or less responsiveness to those gibberellins

This might help to explain some of the observations that don’t fit the simple, single gene, dominant vs. recessive theory.

Just my latest thinking, for what it’s worth.

Best wishes, Tom

I always felt it was hormonal. How it all works is beyond me, though. And how genetics play a part? Who knows… Animal hormones are easier to understand =/ At least there is more research on it for it to be easier to understand.

When I was at uni we did a lab with pea seedlings whereby gibberellic acid was applied to axial buds resulting in the activation of these buds and faster more elongated growth… maybe if gibberellins were applied to the buds of these rugosa seedlings one might be able to induce early flowering to speed up the selection process.

Andy Roberts et al. paper on GA and repeat bloom is great. I had the opportunity to visit with him in person about it in 2005. THere are a lot of questions yet to answer he admitted. He looked at a single blooming rose and its repeat blooming sport (‘White Pet’) and learned that the major difference was that the repeat blooming sport has a lower concentration of the form of GA he followed. (there are over 120 variations identified now) Lower GA concentrations contributed to bloom and higher concentrations limited it. The one time bloomer had low GA at bud break, but then it quickly spiked, the repeater had consistently low GA throughout the year.

I summarized his paper and added some other thoughts in a Summer 2001 RHA article: Repeat Bloom in Roses

Andy was able to inhibit blooming on spring blooming roses with GA application at bud break.

That’s a great point Tom about sensitivity to GA as well as production of GA all interacting together to get what we observe in terms of flowering. There is definately some relatively dominant component that seems to allow for fall repeat to some degree in Rosa laxa descendants and some cultivars like with ‘William Baffin’ where we frequently get one time bloomers from them with crosses to repeaters suggesting they have the one time bloom allele in them that is being trumped a bit by something else.

An idea I had that I thought would be really neat if possible, is to utilize some sort of GA inhibitor. We can treat tissue and hopefully get the appropriate GAs below the threshold of concentration for whatever GAs involved to get one time bloomers to bloom at will. There are GA inhibitors for height control in bedding plants, but the problem is that we probably will have a hard time controlling them enough to get below the threshold in the acutal growing point for flowering and not mess internode length and other things up. It would be worth playing with. It may help us push through generations of breeding with one time bloomers and also just see what kind of blooms they produce and select early on.

Just some thoughts.


White Pet sported from Adelaide d’Orleans. I tried buying it from Sequoia right before they closed but was sent Adelaide Hoodless instead. “Everything happens for a reason”… so I let it go.

Hi David,

“there are over 120 variations identified now” [of gibberellins]

That could explain some of the unexpected results from species crosses too. I’m sure that the different species must have different profiles of all of the various forms of GA. Stirring up the metabolic pot, by hybridization, could result in all sorts of previously unknown combinations.

“The one time bloomer had low GA at bud break, but then it quickly spiked, the repeater had consistently low GA throughout the year.”

This raises some more questions… what triggers the spike in the once-bloomer? And could this trigger be fundamentally different (temperature, daylength, etc.) for different once-blooming species?

Interesting stuff!

Thanks, Tom

This paper may be of interest to this thread: