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 ..

Mutations of genes in synthesis of the ..
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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!)

dendrorhous, particularly for genes involved in the synthesis of carotenoid precursors, such as HMGR, idi and FPS.
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Mutations of genes in synthesis of the carotenoid precursors of ABA lead to pre-harvest sprouting and photo-oxidation in rice.
Photo provided by Flickr

Journal of Investigative Dermatology

Codominance and Incomplete Dominance
We should dismiss Mendel's concept of "dominant" and "recessive." Instead, we should understand it all in terms of whether the organism has functional enzymes or not. This correct interpretation carries us further.
The human ABO blood group gene shows this process clearly. We have a gene that mutated to produce antigens on the surface of red blood cells. Those who inherit this allele have enzymes that synthesize a specific antigen; hence "type A" blood. Those without have "type O." The gene mutated again to produce an allele specifying a different sequence inthe enzyme, different antigens, and "type B" blood. If one inherits both alleles, onemakes both antigens and has "type AB" blood. It's called "codominance," althoughthere's no "dominance" about it. It's exactly what one would expect; the mutant allelesand their enzymes function independently. Neither actually "dominates" the allele thatdoesn't produce antigens, or each other. It's the immune system that says these areantigens, not the red blood cells. It just doesn't object to the cell surface proteinsproduced by "Type O."
The genes Mendel discovered in peas demonstrated simple dominant and recessive characteristics. White crossed with purple produced all purple progeny. Theyget the enzyme, synthesis proceeds, color is produced, end of story. But this is notalways found. In snapdragons and fouro-clocks, crosses of white with crimsonproduce pink progeny. Interbreeding heterozygous F1 pink progeny produces white, pink, and crimson in the expected 1:2:1 ratios in the F2. In these cases the crimson allele is "incompletely dominant" over the white allele in Mendelian terms. Today we can explain it as the homozygous crimsons have two genes producing twice as much enzyme, more color, than the heterozygotes.
We have evidence the genes for pH work this way. It's reported petunias have as many as six genes that affect petal pH. Each acts independently and the final effect is a combination of distinct alleles acting. Remember, this is not like mixing paint! There would be 64 combinations, 64 hues if six genes were acting and each allele had equivalent effect. That's a lot, but still representing discrete differences, not a continuum. We don't know how many genes rhodies have. It's not unreasonable to suggest rhodies have "several." We'll only discover those in which there is variation in the alleles. We also don't know if each allele contributes the same increment of pH change, but that certainly must be the initial hypothesis. Okay, we have questions. Let's find some answers! A scientist would use a pH meter for measurement, but in my experience our eyes are exquisitely adapted for making such fine distinctions and divisions - better than any meter. I selfed deep purplish red 'Dan's Early Purple' and got several repetitions ofdistinct hues from vivid purplish-red to vivid reddish-purple. We should expect there to be distinct differences. How many distinct hues can we find between bright red and our bluest purple? They wouldn't necessarily have to be related (though a good cross might reduce the variables). Could we do it at a show?

Light induction of carotenoid biosynthesis genes in the green alga Haematococcus pluvialis: regulation by photosynthetic redox control.
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Pancreatic Adenocarcinoma — NEJM

Regulation of two carotenoid biosynthesis genes coding for phytoene synthase and carotenoid hydroxylase during stress-induced astaxanthin formation in the green alga Haematococcus pluvialis.

Mutations of genes in synthesis of the carotenoid precursors of ABA lead to pre-harvest sprouting and photo-oxidation in rice.
Photo provided by Flickr

Expression of carotenoid biosynthesis genes during …

ABA is involved in several specific processes during seed development, such as the deposition of storage reserves, induction of primary dormancy. Evidence for the role of ABA in such processes has come from ABA-deficiency or -response mutants in Arabidopsis or maize. Mutations in ABA biosynthesis fail to induce seed dormancy and exhibit a vegetative wilty phenotype, such as Arabidopsis aba1 and tobacco aba2 are known to be impaired in ZEP (zeaxanthin epoxidase), the first enzyme identified as an ABA biosynthetic enzyme; The Arabidopsis ABA-deficient mutant aba4 was recently identified in a screening for paclobutrazol-resistant germination and showed impairment in NSY (neoxanthin synthase). The maize viviparous14 (vp14) and tomato notabilis mutants are shown to be defective in NCED, 9-cis-epoxycarotenoid dioxygenase catalyzing the oxidative cleavage of xanthophylls, 9-cis-violaxanthin and/or 9′-cis neoxanthin to produce xanthoxin., Arabidopsis aba2 and aba3, maize vp10 and vp15, and tomato flacca and sitiens are typical mutants impaired in the later steps of ABA biosynthesis in the cytosol.– By comparison, ABA-deficiency or -response mutants in rice were scarcely identified. At present we have cloned other three genes from phs mutants besides PHS1–PHS4 genes, and they are all involved in specific ABA biosynthetic pathway. Further detailed characterization with these mutants is underway.