of genes in synthesis of the carotenoid precursors of ABA lead ..
The maize Vp5 gene was found to encode a phytoene desaturase (PDS), and transgenic rice plants harboring the PDS–RNAi construct showed a clear albino phenotype (; ). The maize vp9 mutant and the non dormant-1 (nd-1) mutant of sunflower (Helianthus annuus L.) have mutations in the gene coding for zeta-carotene desaturase (ZDS; ; ). The carotenoid isomerase (CRTISO) gene was cloned from the tangerine mutant of tomato and ccr2 mutant of Arabidopsis (; ). The Vp7/Ps1 gene encodes a lycopene-β- cyclase and is necessary for the accumulation of both ABA and carotenoid zeaxanthin in mature maize embryos; the mutant is easily discernible as it has pink kernels because of lycopene accumulation (). These mutants containing defects in carotenoid precursor synthesis exhibit pleiotropic phenotypes, such as albino or pale green, non-viable seedlings and vivipary, due to deficiencies of carotenoid and ABA.
Mutations of genes in synthesis of the carotenoid ..

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HPLC chromatograms of the wild type and homozygous …
On & Off
It's generally known that every organism has the entire genome in virtually every cell. However, that doesn't mean that all the genes are active all the time. Some are active only periodically, e.g., those involved with seasonal flowering, or with cell division. Consider the production ofpigment we've been exploring. Is there any reason for those genes to be active after the flowers are all produced? It does take energy to produce pigment. It would be to the plant's advantage to switch them off when they aren't needed to color flower petals and attract bees. Sometimes geneswill be "switched off" permanently - the fundamental fact behind stem cell research.
How do we see this in the garden? I'm sure you have. How about picoteed blossoms? As a picotee rhody bud begins to develop all the genes are functioning, making enzymes that will synthesizepigment. Color is deposited in the petals as they grow out. Now, through some "sport" in gene regulation, one gene in this chain is switched off before petal growth is completed. One enzyme required for pigment synthesis, perhaps CHI, is no longer produced. (To say enzymes are catalysts and not consumed by the biochemical reactions they mediate is not to say that once produced they are active forever.) So the blossom has a ring of color on its lips, but a colorless throat. In the natural world this could be a disaster, because bees see the UV absorption ofanthocyanins. But humans find the color pattern fetching. Notice that if the affectedenzyme were F3'H then yellow flavonoids could still be produced. Now we get red/pink and yellow bicolors so common in hybrid descendants. Observe this closely: what was pink becomes yellow, without a satisfying orange at the boundary.
On the other hand, what if the gene was initially off and switched on late? Then we get colored throats and eyes. One gets the impression of a rather distracted plant that forgets what it should be doing. Another example of genes turning on and off are the spots, e.g., those in 'SpatterPaint'. Blotches seem to be an extension of spotting. It seems the genes responsible for pigment synthesis enzymes within the spots and blotches are different from the rest of the petal. Pink or red (anthocyanin) petals with yellow (flavonoid) spots and blotches aren't unusual. Looks like F3'H is involved again. Green spots are even seen. Could that be chlorophyll? That's interesting.
Couldn't pigment enzyme genes being switched-off permanently cause whites? Possibly, I suppose. Loss of pigmentation, white, is common in organisms - cats and rats, roses and roosters - though pure whites, pure white in bud and blossom, seem surprisingly rare in rhodies. Most "white" rhodies seem to have some color synthesis, ineffectual as it may be. Much genetic research over the past century has shown us how gene mutations affect the enzyme systems. Malfunctioning enzymes are a direct result of mutation. Examples of point mutations causing amino acid substitutions in proteins have been found generally.3
What makes 'Yaku Fairy', a 20-year- old tuffet two feet across and a foot high, so different from ssp. that can pop a new branch that grows a foot or two in a summer? It's the same fundamental process as demonstrated here for color. When we look at 'Yaku Fairy', we should think of Figure 1 (Part I) and the way a malfunctioning CHI can stop the entire chain of color synthesis. But this time a malfunctioning enzyme early in the synthesis chain for growth factors, instead of color, stunts growth. Middling-sized plants synthesize more of the chain, and in the synthesis goes all the way. As I wrote early in the prior article, while this has been primarily about color, because it's easier to see, the processes are essentially the same for all characteristics we hybridize. It underlies all our interpretations of what's going on. The process presented here is universal.
Abscisic acid and the pre-harvest sprouting in cereals
Orange
You may have noted I've touched on orange in various ways. If not a true "delphinium blue," elepidote breeders with their yellow and pink bicolors and blends may covet the really bright orangey colors of , , or and the Exbury azaleas more than anything. Elepidote hybridizers have tried to create orange by combining red and yellow. If the yellow were a carotenoid, produced by an independent terpene synthesis chain,that would be easy. Indeed, look at the yellow admixture in ; it could be hard to get out!
I expect 'David' X 'Crest' was done for this reason. Red 'David' X yellow 'Crest' makes reds with no trace of yellow (as seen of JE #256, #487 in the TVARS garden at Jenkins Estate, Aloha, Oregon).'David' provides genes and enzymes that use the precursors of those yellow flavonoids as precursors to synthesize red cyanidin. The same effect is seen in pink 'Airy Fairy' (yellow X pink 'Cornell Pink'). But, "you can't have your cake and eat it too," not an orange.
An inefficient F3'H might be thought to do the trick. Some of the dihydrokaempferol would be converted to eriodictyol and dihydroquercetin leading to some cyanidin, pink in a low-pH petal,leaving some to be converted to yellow flavones and flavonols by FNS and FLS. Theoretically, this way one might produce a blend of yellow and pink, appearing orange. But either way, it seems to have been very hard to do. Now we know why. Not only is this problematic from the way anthocyanins and other flavonoids are synthesized, but think of the combined absorption spectra. Even when something more or less orangey is produced this way, to my eye it lacks the brilliance of the Exbury's. I'm sorry, but getting an impression of orange thirty yards away from a yellow and pink bicolor just doesn't do it for me, even in my seedlings (I can see one out my window as I write this).
If we want true orange in our elepidotes, it would seem we should hunt for fertile azaleodendron hybrids. We could try to get the DFR that can use naringenin from subgenus tomake pelargonidin. Or perhaps we could get carotenoids from them. Tetraploid would be a poor choice for diploid subgenus elepidotes, but perhaps or R. can bring us this allele. (I didn't promise this would be easy!)

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