First draft - Can North American rose hybridizers safely use pollen from PNRSV infected roses?

General Discussion
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This a first draft, all comments, suggestions, questions, etc. welcome (unfortunately, my formatting, use of bold face, etc. was removed when I uploaded the manuscript).

Can North American rose hybridizers safely use pollen from PNRSV infected roses?

By Henry Kuska

First Draft, 2-08-2003

In the 1990s I ran a (free) e-mail rose breeding scientific literature “course”. One of the questions that I received was from a prominent North American rose hybridizer (of All American Rose caliber). He stated that from what he had read rose mosaic virus could not be spread by pollen. However, he had occasionally observed virused roses among his seedlings. He asked if I knew of any scientific rose literature on the subject.

First, I will define my terms. There are a number of viruses that historically have been included under the broad term “rose mosaic virus”. In this discussion, I will limit myself to what, at present, appears to be the most prevalent rose “mosaic” virus in North America, prunus necrotic ringspot virus (PNRSV). A more accurate scientific name is prunus necrotic ringspot ilarvirus, but I will use the more common prunus necrotic ringspot virus.

In the “Plant Viruses Online” database, the (general) modes of transmission for PNRSV are given as: “Transmitted by means not involving a vector. Virus transmitted by mechanical inoculation; transmitted by grafting; not transmitted by contact between plants; transmitted by seed (to over 80% in Prunus pennsylvanica but much less in peach); transmitted by pollen to the seed and transmitted by pollen to the pollinated plant.” (1)

The above is a general statement. It is possible (but not probable) that PNRSV could be transmitted in pollen of other infected plant species (to some non-zero degree) but not transmitted at all (zero) in roses. To see whether this remote possibility of zero transfer is actually the case, specific scientific studies of roses and PNRSV will be examined.

The earliest pertinent studies that I could find were three that were published in 1980.

One was by D. J. Barbara, East Malling Research Station, United Kingdom. She reported that “In rose high levels of virus were present in petals and stamens but only very low levels in the sepals.” Note, for the non scientific reader, pollen is released from the stamens. Also, she is referring to PNRSV. (2)

The second 1980 paper is actually 3 papers published by J. B Sweet, Long Ashton Research Station, University of Bristol,United Kingdom. He reported that PNRSV was detected in the pollen of Peace and Queen Elizabeth roses, and in 1 % of two batches of seedling Rosa multiflora rootstocks. As is typical of scientific caution (or at least should be), he points out that finding the virus in the seedlings is not a definitive proof of transmission through the rose seed. However, his statement should not be interpreted that he did not find non grafted seedlings with virus, it means that he cannot be sure that it came through the seeds; it could of come from infected shears, thrips, etc. after the seedlings were planted. What it does show is that there was transmission of PNRSV to non grafted seedlings in 2 different batches (unless there was experimental error). Since multiflora seedlings are grown together in a field, I think that one cannot use “root grafts to an infected neighbor plant” as a probable reason as you would be going in a circle logically i.e. you would have to explain how the infected seedling that supplied the root graft got infected. In the Journal of Horticultural Science paper, he states: "“Two plants from a batch of about 200 Rosa multiflora seedling rootstocks with mosaic symptoms on their leaves induced PNRSV-type symptoms in the woody indicatore, whereas four symptomless plants did not. Virus was sap-transmitted from one of the mosaic-diseased R. multiflora seedlings which induced typical PNRSV symptoms in herbaceous test plants, and infected cucumber sap-precipated with NRSV-G but not with ApMV-P and PDV-B antisera.”

Note, there is no graft on these infected plants; they are seedlings. Also note, Sweet used a very crude detection systems (visual symptoms), we do not know how many more of the 194 were infected but did not show symptons. Even of the 4 symptomless plants that he tested and that were negative, we do not know if any of them would have tested positive with todays’ much more sensitive procedures. This paper is a very important one relative to the topic being considered! (3)

The third 1980 paper was published by B. J. Thomas. He found that both the gel immunodiffusion test and the latex test were unable to detect PNRSV in infected roses but that both ELISA (enzyme-linked immunosorbent assay) and SSEM (serologically specific electron microscopy) methods were able to (in some cases ELSIA also failed). SSEM was twice as sensitive as ELISA. Of particular importance here is that he was able to detect the virus in the the rose stamens. (4)

The next two papers are also very important to this discussion as the first reports (and the second confirms) that it is possible to “transfer the virus by mechanical means”. This is an important finding because this removes the possibility that the virus is “too fragile” to be transferred by anything but a graft (living phloem cells of the plant). The “too fragile” theory seems to be a key assumption of the “no transmission but by grafting” school of thought.

The first report of mechanical transfer was in 1981, by B. J. Thomas. He reported that his preliminary attempts to transfer the virus by mechanical means failed, but by adjusting his experimental procedure he was successful - including the use of infected rose petals and anthers (it is not clear if the petals and anthers were mixed together or tested separately). (5)

The ability to transfer the virus by mechanical means was confirmed in 1994. H. Baumgartnerova, Institute of Experimental Phytopathology and Entomology, Slovak Academy of Sciences, Czechoslovakia reported that the virus was positively mechanically transmitted from diseased leaves and pollen of roses. (6)

In fairness to possible overlooked articles, I should point out that my search may not be complete as computer abstracting searches are relatively recent; and there may be articles in relatively small scientific journals that have not yet been covered by the abstracting services nor referenced in the articles that I have cited. However, I feel that the above six set of articles provide sufficient information such that North American rose hybridizers should be wary of using PNRSV diseased roses as pollen parents in their hybridizing program.

Examples of how others have interpreted the literature up to the date of publication of their own work are given next.

In the 1983 book “Compendium of Rose Diseases” by R. K. Horst, Professor Horst (Cornell University, Plant Pathology) wrote: “PNRSV is pollen-transmitted in fruit trees. Pollen transmission is suspected to occur in roses also. Since spread in the field is slow.” (7)

Baldo Villegas (Associate Environmental Research Scientist (Entomologist),California Department of Food and Agriculture) consulted with the following plant pathologists with the California Department of Food and Agriculture’s Plant Pests Diagnostic Centre: Dan Opgenorth and Dennis Mayhew before preparing his web page article on the subject. He stated: " They have given me invaluable advice in preparing this article." Regarding spread, he stated: “Some pathologists suspect that mosaic may be pollen transmitted which could prompt removal if other roses in the garden are valuable and not already infected”. (8)

In 1989 in an article titled “Incidence of Rose Viruses in Spain” M. Cambra, J.L. Martinez-Torres, M.J. Benaches, E. Camarasa, and M.T. Gorris studied 4,730 rose samples. They found 4.2% of the roses had PNRSV. The breakdown was: 44.0 % of the minatures, 1.1 % of the hybrid teas, and 1.5 % of those budded on Manetti rootstocks. Cambra et.al. state: “The high rate of PNRSV contamination in minature varieties seems to be associated to their long existence.” Later in another paragraph they say:“…since this virus is pollen transmitted (in addition to grafting).” They also suggest that one way to prevent the virus from spreading is to prevent the plants from flowering. (9)

Professor Gerald C. Adams (Department of Plant Biology and Department of Plant Pathology, Michigan State University) makes the following statements: “Rose Mosaic Virus in the Americas is most commonly caused by prunus necrotic ringspot virus which is a pollen transmitted virus but transmission by pollen is very low. When transmission by pollen does occur it is usually due to a high population of thrips. The thrips carry the pollen or infected sap and introduce it into a feeding scar on a leaf or petal.” Farther in the article he states: “Spread of PNRSV by pollen is measurable in cherry orchards and the virus has been found to exist at high titer in rose stamens. Never the less, field spread in rose nurseries has not been easily demonstrated and apparently is rare. In fact most spread of PNRSV is by grafting during vegetative propagation.” (10) I included the second quote for completeness, but please remember that the focus of the present paper is spread in hybridizing, not field spread.

Unfortunately, nature often is not as simple to understand as we would like. This appears to be one of those times as there are 2 papers that looked for PNRSV transfer to seedlings through pollen but did not find it.

The first paper is Sweet’s Journal of Horticultural Science paper referred to earlier. He germinated seeds from the two infected plants (36 seedlings from one and 24 seedlings from the other. None showed visual symptons and 5 random samples from each were grafted on P. Persica GF 305 seedlings (virus test plants) and did not test positive. There are several reasons that I do not consider this report definitive: 1) 10 grafting tests is too small a sample size, 2) the use of visual symptons on 36 samples can now be considered as both too small a sample and to be deficient in test sensitivity, and 3) if the infected bushes were among the 198 "healthy ones; it is possible that the pollen came from the healthy bushes since many (most, all?) pure species roses are self sterile (see discussion 2 paragraphs down).

The second virus-seed transmission test paper was published in 1984, by B. J. Thomas. (11) He reports on three different experiments that could provide some information regarding virus-seed transmission. In the first experiment he crushed 10 seeds from each laboratory infected virused plant with hips, and could not, using ISEM, detect any PNRSV in the seeds (he did not state the number of batches examined). In the second experiment he examined, with ISEM, 1067 seedlings grown from seeds harvested from the infected bushes and found no PNRSV infected plants. A possible explanation for the failure to detect PNRSV in the seeds or resulting seedlings is that the seeds may have also (like Sweet’s samples) been unintentionally produced from non-infected pollen. The following is Thomas’ description of the plantings: “Seed was collected for 3 yr from virus infected plants planted in nematode-tree soil 50 cm apart in two rows 2 m apart so that plants of the same species were opposite each other. A row of corresponding healthy roses were planted equidistant between these rows.” The roses utilized were all species roses, R. canina, R. canina, var. Brogs, R. corymbifera, R. multiflora, and R. Rugosa. If we accept the self sterile model, the seeds that he should of been examining were the ones on the non virused bushes between the two infected ones. (His experiment may still be valid if the neignboring plants in the same “infected” row were of the same species and also had PNRSV - I have to add the “also had PNRSV” because he had plants with 3 different virsus in the study - the neighbors could have had one of the other 2 viruses. This information was not given. Also, except for R. rugosa, the other species roses are once bloomers, and the bloom periods for the same row infected neighbors may possibly not have overlaped the bloom period of the one between in that row. In the third “experiment” he did detect PNRSV in three seedlings of new rose cultivars (planted in the Royal National Rose Society’s trial grounds). One infected plant was of unknown origin, one was from France, and one was from the USA (via France). Since the hybridizing, growing conditions, were not controlled (for example, was a virused rootstock used?), the results from this third “experiment” are not scientifically of value relative to the present question.

This paragraph discusses the literature evidence for the self sterile model. In 1986 P. Cole and B. Melton published a paper which investigated the ability of rose pollen to fertilize flowers on the same bush. (12) The diploid species were all highly self steile. None of the 23 diploid specimens exhibited over 4 % fertility and 18 of the 23 produced no self-set seed. They also studied the fertility with pollen from another plant of the same species and found that the diploid group was 50 times more cross compatable than self compatable. For roses of higher polyploid level 12 of the 16 studied were no more self compatible than the diploid group. Unfortunately, only two of the species studied by Thomas was also studied by Cole and Melton, one was R. rugosa which was 100 % self sterile, and the other was R. rubiginosa Linnaeus (R. eglanteria) which was 83.4 % self sterile (one sample). Thomas’ R. canina, R. canina var. Brogs, and R. corymbifera are of the canina section as are two of the species studied by Cole and Melton. One is R. horrida Fisch. which was found to be 100 % sterile and the second is R. laxa Froeb. which was one of the least self sterile species studied, only 55 % self sterile. It should be noted that only one plant of R. laxa Froeb. was available for this study. In the other case of low self sterility R. engelmanni, one sample was 54 % self sterile while four other samples of the same species were 100 %, 99 %, 100 % and 100 % self sterile. Thus, the R. laxa Froeb. low self sterility number may not be representative of the species, but actually due to having an individual plant that has some other species in its ancestory.

A very recent paper by Han YounYol and Yu SunNam (13) did confirm that R. Rugosa was self sterile but reported that R. multiflora did self fertilize. I posted a request for members of the Rose Hybridizing Association to check to see if they had information on the question of whether R. multiflora is self sterile. David Zlesak stated that" roses have a gametophytic self incompatibility system which can be easier to break down than a sporophytic system…" John Moe replied that he had an isolated R. multiflora that did not have any hips all season. Jim Turner reported a few hips, but his bush was not isolated (he reported an early spring blooming, one textbook source reports a July blooming?). Paul Barden reported 2 separated bushes had many hips. The bushes were not isolated from other roses. He had grown seedlings from the hips and the seedlings looked like they were only R. multiflora. Possible complications that may explain Paul Barden’s results include: 1) apparently first generation crosses with species roses often look like the species rose. It is not until the second generation that major differences appear, 2) it is possible that a small amount of compatible pollen (from a neighboring bush) may break the barrier for pollen that would normally be incompatable, and 3) Paul’s R. multifloras may already have some foreign blood in them as over the years rootstocks have been selected for various characteristics such as lack of thorns.

There is a very recent paper which I am including for completeness, but it does not specifically address the pollen issue. It is a 2001 paper by Benoit Moury, Loic Cardin, Jean-Paul Onesto, Thierry Candresse, and Alain Poupet. They report that 4 percent of cut-flower roses from different European sources were infected with Prunus necrotic ringspot virus (PNRSV). The abstract reads: “Progression of the disease under greenhouse conditions was very slow”. Now, the abstract is all that most scientists will read so most (all?) authors proofread it very carefully - in other words I would not expect an error in a abstract. However, in the article the following appears: “Our observations show that the progress of PNRSV infections in roses grown in greenhouses is very slow (or nonexistent), because in our trial only 1 % of the plants were PNRSV infected 2 years after planting (without taking particular cautions for isolation of the plants or disinfection of the tools used for pruning).” (14) What is confusing to me is the addition of the “(or nonexistent)” which does not appear in the abstract.

A possible reason that the spread is very slow through seed transmission is that the PNRSV appears to be on the surface of the pollen and in the part of the pollen that forms the pollen tube but not in the actual “sperm”. (15)

A definitive experiment is to hand pollinate a fertile isolated rose (that has had its own pollen removed) with diseased pollen from an infected rose that is known to cross with it. The pollinated flower would then be covered to prevent stray pollen from contaminating the experiment. This would check for seed transmission.

Reference (1) http://image.fs.uidaho.edu/vide/descr658.htm , Brunt, A.A., Crabtree, K., Dallwitz, M.J., Gibbs, A.J., Watson, L. and Zurcher, E.J. (eds.) (1996 onwards). `Plant Viruses Online: Descriptions and Lists from the VIDE Database. Version: 20th August 1996.’ URL http://biology.anu.edu.au/Groups/MES/vide/ Dallwitz (1980) and Dallwitz, Paine and Zurcher (1993) should also be cited.

Reference (2) Barbara, D., J., Acta Phytopathologica Academiae Scientiarum Hungaricae, volumn 15, pages 329-332, (1980). Reprinted in Acta Horticulturae, volumn 94, published March 1, 1981.

Reference (3) Sweet, J., B., Acta Phytopathologica Academiae Scientiarum Hungaricae, volumn 15, pages 231-238, (1980). Reprinted in Acta Horticulturae, volumn 94, pages 231-238, (1981).

Http://www.actahort.org/books/94/94_31.htm

He published a similar (but not just a duplicate) paper in: Journal of Horticultural Science, volumn 55, pages 103-111, (1980).

Reference (4) Thomas, B. J., Annals of Applied Biology, volumn 94, pages 91-102, (1980).

Reference (5) Thomas, B.J., Annals of Applied Biology. volumn 98, pages 419-429 (1981).

Reference (6) Baumgartnerova, H., Acta Horticulture, volumn 377, pages 357-359, (1994). ROSA SP. - RESERVOIR OF THE SOUR CHERRY NECROTIC RINGSPOT VIRUS

Reference (7) Horst, R., K., book “Compendium of Rose Diseases”, published by The American Phytopathological Society, St. Paul, Minnesota. pages. 26-27, (1983) .

Reference (8) Baldo Villegas web page, http://members.tripod.com/buggyrose/ipm/83rosemosaic.html

Reference (9) Cambra, M., Martinez-Torres, J.L., Benaches, M.J., Camarasa,E., Gorris, M.T., Acta Horticulturae, vol 246, pages 309-312, (1989).

Reference (10) Adams, G., C, “Rose Mosaic Virus in the Nursery”, http://extension.bpp.msu.edu/rosemosaic/ , last revised 9/7/2002.

Reference (11) Thomas, B., J., Annals of Applied Biology. volumn 105, pages 213-222 (1984).

Reference (12) Cole, P., Melton, B., J. Amer. Soc. Hort. Sci., volumn 111, pages 122-125, (1986).

Reference (13) YounYol, H. and SunNam, Y., Journal of the Korean Society for Horticultural Science, Volumn 43, pages 326-332, (2002).

Reference (14) Moury, B., Cardin, L., Onesto,Jean-Paul, Candresse, T., Poupet, A., Phytopathology, Volumn 91, pages 84-91,(2001)

Reference (15) Aparicio, F., et.at., European Journal of Plant Pathology, volumn 105, pages 623-627, (1999).

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I posted (Saturday evening) without running the paper through a spell checker. At 12.07 a.m. Sunday morning Peter Harris e-mailed me a long list of suggested English changes (he is a college English Professor in his “other” life).

Rather than my submitting a whole new draft at this point, will those of you that are willing to act as “on-line editors/referees” of this draft please concentrate on comments concerning the science that has been presented as well as comments on how to improve the clarity.

I have now found several references that say that multiflora is a June bloomer and one (Modern Roses 11) that says that is a summer bloomer.

Thank you,

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How soon are you submitting your article? I’ve seen references to R canina and R eglanteria being self fertile. I think I saved copies, but this was 5-some odd years ago and my filing system is basically non-existant. From personal experience, I’ve got two plants of R. canina right next to each other. Both are cuttings off of the same parent plant. They always have lots of hips on them, and the year I bagged some buds, I got decent hip set off of the bagged blooms. (Not quite as many seeds as the OP hips, but I also had rotting petals left in the bags, which could have played a role.)

I believe there is also an article on either Karl King or Paul Bardon’s website regarding fertility of North American rose species. I beleive the author’s last name started with E (Erl…?). It was copied from another printed source.

Joan

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Joan, in a sense it is already submitted as Peter Harris is the new editor (at least that is my understanding), and I consider everyone here as a referee.

This posting of the draft is not his idea; this is my idea. It should not be considered as a precedent or an indication of his editorial policy, i.e. I did not discuss doing this with him.

It may also appear on my web site and at least one other hybridizing related website (it is in the public domain).

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Timing of multiflora bloom is dependent of where the multiflora is growing.

Last spring, it was blooming in Williamsburg Virginia in latest March.

In my part of Tennessee, it blooms early, late April or early May.

Going up the Shenandoah Valley of Virginia, it blooms around memorial day in Staunton.

I’ve got a list of relative bloom times, but the timing of the beginning varies with dates of latest freezes.

Ann

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Professor Eileen Whitehead Erlanson in her article “American Wild Roses”, published in the 1932 edition of the American Rose Annual makes the following statement: “In Rosa there are both types of species; stable, well-defined systems such as Rosa laevigata, and enormously variable complexes such as R. multiflora and its relatives.”

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Joan,

Was this the article you were thinking of?

Link: www.rdrop.com/~paul/american.html

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Thank you Paul, that was the article I was thinking of.

Joan

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Although 4% fertility is surely not very good compared to what it might be, it might be good enough, given the tremendous number of pollen grains produced.

I could mention a number of species roses I’ve grown which regularly produce self-pollinated seed. One of these is R. hugonis, almost always the first to bloom. Although it is not prolific as a seed-setter, it usually has 15-20 hips on it. These hips are surely from self-pollination (unless pollen from maples is helping…) since there are no other roses in bloom at this time.

Regardless of the level of self-fertility in this range from sterile or nearly sterile to fairly fertile, it might be useful to consider the effect of PNRSV on the pollen produced by the infected plant. In the various articles cited, I don’t remember any discussion specifically related to whether the virus might decrease the viability of the pollen produced, perhaps causing pollen to be sterile/non-functional. Near the end there is one comment (credited to Aparicio) that might be related to this issue:

A possible reason that the spread is very slow through

seed transmission is that the PNRSV appears to be on the

surface of the pollen and in the part of the pollen that

forms the pollen tube but not in the actual “sperm”. (15)

Does Aparicio deal with virus as a cause of decreased fertility? If virus does decrease fertility, then maybe the risk to us is even less than might be predicted through the presence of the virus in the pollen grains.

As for the slow-or-nonexistent spread of the virus in greenhouses, I’d expect that the presence/absence of insect vectors might account for such a small number of cases.

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Comments on Peter Harris’s comments.

PH said: Although 4% fertility is surely not very good compared to what it might be, it might be good enough, given the tremendous number of pollen grains produced.

Reply: The 4 % fertility is the maximum reported by Cole for dipold fertility. This small number is probably consistent with the following observation cited in the pollen behavior thread: “that the pollen cells mature before the embryo sac and egg cells. Most of the pollen is shed when the petals first open and insects will carry some of it to flowers opening for the second day, which may then be ready for cross-fertilization. However, a few pollen grains remain on the shriveled anthers on the third day and the stamens should still be receptive.”

We are interested in whether the major type of pollination (for the virused roses under the experimental conditions reported in the 2 papers that did not find spread) was self or neighbor pollination. Both of these observations suggest neighbor pollination while the authors assumed self pollination. This ambiguity would be settled by my suggested “definitive” experiment of directly placing infected pollen on a flower that has had its pollen removed. This experiment is also exactly what a hybridizer does. If this experiment finds spread, then others may want to re-study the more complex issue of field spread.

PH said: I could mention a number of species roses I’ve grown which regularly produce self-pollinated seed. One of these is R. hugonis, almost always the first to bloom. Although it is not prolific as a seed-setter, it usually has 15-20 hips on it. These hips are surely from self-pollination (unless pollen from maples is helping…) since there are no other roses in bloom at this time.

Reply: R. hugonis is one that Cole found to be self-sterile so obviously Peter has the first maple-rose crosses in the world (or his plant has some mixed blood or Dave Z.'s comments apply).

PH said: Regardless of the level of self-fertility in this range from sterile or nearly sterile to fairly fertile, it might be useful to consider the effect of PNRSV on the pollen produced by the infected plant. In the various articles cited, I don’t remember any discussion specifically related to whether the virus might decrease the viability of the pollen produced, perhaps causing pollen to be sterile/non-functional. Near the end there is one comment (credited to Aparicio) that might be related to this issue:

A possible reason that the spread is very slow through seed transmission is that the PNRSV appears to be on the surface of the pollen and in the part of the pollen that forms the pollen tube but not in the actual “sperm”. (15)

Does Aparicio deal with virus as a cause of decreased fertility? If virus does decrease fertility, then maybe the risk to us is even less than might be predicted through the presence of the virus in the pollen grains.



Reply: The PNRSV infected pollen from closely related plants does produce infected seedlings so I doubt that the infection would kill the rose pollen. This would be easy to check. One needs only a microscope and some readily available household chemicals like sugar to check for pollen germination (or simply pollinate with infected pollen and see if a hip forms). Whether an infection would make the pollen, say, 10 % less effective than healthy pollen is a possibility that would require a complex experiment. Since the point under discussion is whether hybridizers should use infected pollen, a X % reduction makes no difference as the hybridizer has removed any competing healthy pollen.

PH said: As for the slow-or-nonexistent spread of the virus in greenhouses, I’d expect that the presence/absence of insect vectors might account for such a small number of cases.

Reply: in other words, infected pollen that does not reach the plant does not cause spread.

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“This ambiguity would be settled by my suggested “definitive” experiment of directly placing infected pollen on a flower that has had its pollen removed.”

I agree. This experiment would be useful. Any volunteers?

“R. hugonis is one that Cole found to be self-sterile so obviously Peter has the first maple-rose crosses in the world”

Bummer. I’d love to market this amazing variety, but my bush died last year. :frowning: Still, maybe some of the seeds will germinate this spring. If so, I’ll be taking orders for plants.

“in other words, infected pollen that does not reach the plant does not cause spread”

True. And pollen is not the only possibility. In the absence of insects or other vectors, infected plant juices will not be transmitted from one plant to another by the vectors. Re. the report–the infections (if there were any) might have come through either route–or via shears, since there was no attempt to prevent such transmission. As you implied, the report’s implications aren’t really clear.

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My multiflora’s early bloom may be due to the mild climate (no frost most years) and the fact that I don’t prune it. It never goes dormant. I prune most of my roses in January, which generally makes them go dormant, but I don’t prune the multiflora.

I wonder if the maple-rose cross will give good Fall color? :wink:

So Henry, will you be doing the definitive experiment?

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Jim said: "I wonder if the maple-rose cross will give good Fall color? :wink: "

I hope so. Since the likely pollen parent is a sugar maple about 50 feet tall, these “mose” trees should be large enough to make a good display when they bloom in the spring. Already I’m imagining 6" bright yellow blossoms with red stamens (non-virused pollen, of course), the blossoms to be followed by apple-like hips. No self-sterility here.

I’m hoping also that the sugar will be pleasing to the palate. Tapping the sap and boiling it down to syrup will be a good springtime activity for my grandchildren–as soon as Henry sends me some (my children don’t have children yet). It could be big business–tourism, mose candy, mose shows with trophies, etc. Devotees could log on to http://www.ams.org to check show results and learn better ways to grow giant specimens and cover up the bare trunks with plantings of herbs and lower-growing varieties of mose.

Large prickles on the branches will not cause problems because they will be respected by mosarians and pests alike, and disease will not be a problem because the pollen parent and the seed parent are almost immune to blackspot, and like all children, moses will inherit all the best qualities of their parents and few or none of the bad qualities.

The only down side I can see (and I concede that this could be a real letdown) would be the tendency of some gung-ho exhibitors to fall out of trees while gathering blossoms they hope will win the Queen of Show award. This problem would decrease over time: succeeding generations of mosarians would be less likely to meet such a fate because those who descend in such a way are less likely to have descendants.

Peter

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Jim, in my garden I do not have any virused roses (from visual inspection) to take the diseased pollen from. Plus, there is the problem of credibility. Normally, independent verification or non-verification is preferred. The “verification” (either way) by one of the interested parties is often considered not definitive. The optimum verification would be by a independent laboratory that has access to SSEM testing facilities.

If I see an obviously virused non species rose (or roses) in a public garden, I will probably ask for some of its (their) pollen and place the (mixed) infected pollen on one of my roses that I know sets lots of hips like Carefree Beauty. I realize that I am running the risk of passing the disease to Carefree Beauty, so before I would do that, I would start a cutting of Carefree Beauty. I would then look for virus markings in the seedlings. If I am “lucky” I would see a diseased seedling. But, if there are no visible symptoms, I doubt that my wife would approve the cost involved in purchasing ELISA test kits. :>)

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Peter, I think Paul Barden’s crosses with telephone poles are more important. What could add more disease resistance and winter hardiness than a telephone pole?

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I was meaning to ask about Paul’s telephone pole crosses. Can you imagine the ease of just planting a seedling where you want the telephone pole to be. Especially in our area where you usually have to use dynamite to get the required depth. I was wondering if Paul wasn

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The following is a revision of one part of the manuscript (again the uploading removes formatting):

A very recent paper by Han YounYol and Yu SunNam, see footnote (13) did confirm that R. Rugosa was self-sterile but reported that R. multiflora did self-fertilize. I posted a request for members of the Rose Hybridizing Association to check to see if they had information on the question of whether R. multiflora is self-sterile. David Zlesak stated that" roses have a gametophytic self incompatibility system which can be easier to break down than a sporophytic system…" The reports from the RHS members were varied. They ranged from definitely sterile, a few hips, to reports of many hips. These results appear consistent with David Zlesak’s comments.

The self-sterility issue may not as important to this investigation as I first thought. In the 1963 American Rose Society Rose Annual, Dr. Eileen W. Erlanson Macfarlane, see footnote (14) makes the following statement concerning the self-pollination mechanism in roses (not an exact quote, the structure changed to include only the part pertinent to this discussion): “It was found that the pollen cells mature before the embryo sac and egg cells. Most of the pollen is shed when the petals first open and insects will carry some of it to flowers opening for the second day, which may then be ready for cross-fertilization. However, a few pollen grains remain on the shriveled anthers on the third day; and the stamens should still be receptive.”

Thus, even if the infected plant is not self-sterile; the pollen from the nearest neighbor non-infected plant of the same species would have the first opportunity to pollinate the infected bush (assuming that bees were around, which should be a reasonable assumption since the studies were done in an open field).

A possible reason that field spread may be slow through seed transmission is that the PNRSV appears to be on the surface of the pollen and in the part of the pollen that forms the pollen tube but not in the actual “sperm” (the study was on PNRSV in nectarine pollen). See footnote (15). The authors of that study comment: “However, the possibility that sperm cells are infected during or after mitosis, before fertilization, cannot be ruled out. In addition, it is also possible that PNRSV could be transmitted by the vegetative cytoplasm of the pollen, which contains high amounts of the virus…Recent evidence indicates that during fertilisation some male cytoplasm can be transferred into the egg cell…”.

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QUESTION. I have not included the information that PNRSV has been detected on honeybees and in their hives. Do you think that I should?

18

I suspect that Paul is keeping his telephone pole crosses hidden for now as I assume that they give his roses teriffic long, straight stems that should easily win many Queen of Show awards.

19

Henry, you need to use html formatting if you want it to look right on a web page. Microsoft Word and other word processing programs allow you to export a document as html, retaining the formatting. Some do a better job of it than others. It’s such a pain to do that I don’t recommend it.

20

I’m confused about the exact crosses and experiments you are planning. I assume that the goal is to find an infected plant, obtain selfed progeny, and then see if the virus is found in the seedlings. One can try to get around self-incompaibility if need be by using a very warm greenhouse or early or late pollinations. Also perhaps GA applications here would be valuable to allow more time for slower self-incompatible pollen to reach the ovule.

Wouldn’t a stronger test to see if the virus is pollen transmitted to cross pollen from an infected parent onto a clean parent? You don’t have the confounding factor of the possibility of virus being transmitted through the egg. Of course one would risk infecting your clean female parent. If some of the seedlings are infected (and of course we assume they will be isolated to rule out post germination infection) the source of the virus should be the infected pollen.

Since roses have a gametophytic self-incompatibilty system (there are a number of scientific references you can find to document this), any rose that is pollinated with an infected male runs the risk of infection-compatible or incompatible. In a gametophytic system the pollen germinates and the pollen tube forms. Incompatibile combinations just have the pollen tube grow slower and often become arrested. All that is necessary for female infection is transmission of the virus from the pollen tube to the style and then from the style to the rest of the maternal plant.

David