For many crops, you don’t have to search very far to find a nice summary chart of the major genes involved in economically important traits. This kind of information makes breeding decisions a lot easier. Knowledge of the genetics underlying traits allows the breeder to identify varieties that are homozygous for a particular trait and to use those varieties to produce predictable progeny. Unfortunately, no such thing exists for potatoes as far as I have seen. This surprised me, because the potato is one of the most studied of all food crops. However, the potato also doesn’t have the same kind of following among amateur breeders as do crops like tomatoes, peppers, and corn, so there is less demand for easily digestible information.
That leaves the scientific literature and there is plenty of it. Unfortunately, much like the taxonomy of potatoes, there are multiple systems that have changed with time and that also have been applied differently for diploids and tetraploids. I’ve done my best to pull together the most current information here in a way that unifies the treatments of both diploids and tetraploids. Where there are popular alternatives, I’ve noted them. Diploids and tetraploids have the same genes, but some of them may not function in the same way in tetraploids, where additional copies of the gene can result in the trait almost always or almost never being expressed, or being expressed in an intermediate form.
Potatoes make life complicated for the breeder in several ways:
Many potato traits are quantitative rather than qualitative. Qualitative traits are well represented by classical, Mendelian loci. Quantitative traits are determined by the interactions of complexes of quantitative trait loci (QTLs). What’s the difference? At the biochemical level, these are really the same thing, but the outcome that the breeder experiences is quite different. A Mendellian locus controls a single trait in a dominant/recessive regime. A good example of this in potato is the P gene. Dominant P* turns on purple anthocyanidin production and recessive pp turns it off. While you may not get purple tubers even with dominant P due to the involvement of distribution genes, you will never get purple tubers with recessive pp. A QTL is usually part of a group of loci that collectively determine a particular trait. A good example of this in potatoes is yellow flesh. Yellow flesh is primarily controlled by the Y locus, but intensity is affected by at least half a dozen QTLs. I have avoided delving into quantitative traits in this post because the available information would be hard to summarize in a useful fashion. The major qualitative traits are of primary interest to the amateur potato breeder.
Another problem is the presence of multiallelic loci. Multiallelic loci contain three or more alleles and therefore cannot be analyzed in the binary fashion used for the more common biallelic loci. B is an example of a multiallelic locus, with five alleles identified to date. Typically, these alleles operate in a winner take all fashion, with the highest valued allele taking the dominant position, but unusual things can happen with increased dosage in polyploids.
There are two main types of color genes: those that control the production of a pigment and those that control the distribution of a pigment. The following table summarizes the main qualitative color genes in the potato and their interactions.
Summary of Qualitative Loci Operating in Diploid and Tetraploid Potatoes
|B||Bd/Bc/Bb/Ba/b||10||Controls distribution of pigmentation to flower abscission zone (Ba-d), eyebrow (Bb-d), seed spot (Bc,d), and petiole base (Bd). Recessive bb blocks color distribution to all of these locations.||Only functions with dominant P or R, as pigments are otherwise not produced, so cannot be distributed.|
|I (D)||I/i (D/d)||10||Controls distribution of color to tuber skin. Intensity of color may be in part dosage dependent on I, so tetraploids can display wider gradation.||I is often used when discussing diploids and D for tetraploids, but they seem to be converging in modern work. E/e has also been used and appears to be nearly synonymous. In diploids, I is epistatic to Pf; neither skin nor flesh color will develop with recessive ii. Sometimes divided into Ico and Iep, for cortex and epidermis, respectively, although this doesn’t appear to be commonly used.|
|F||F/f||10||Distribution of color to flower||Only functions with dominant P or R, as pigments are otherwise not produced, so cannot be distributed.|
|M||M/m||?||Restricts skin pigmentation to the eyes when I is dominant.||Some sources consider this dubious, although it does explain colored eyes in some tetraploids that have white skin but dominant P or R.|
|Y||Or/Y/y||3||Orange and yellow flesh||Controls production of the pigments lutein (yellow) and zeaxanthin (orange). Some sources suggest that these may be separate loci (more about that below).|
|P||P/p||11||Purple/blue pigmentation (anthocyanins; petunidin derivatives)||P is epistatic to R; more purple pigments are produced than red, even when R is also dominant. It is important to note that red pigments are not turned off, just produced in lesser amounts.|
|Pd||Pd/pd||?||Controls distribution of pigmentation of the top sides of leaves||Used with diploids; unclear how it applies to tetraploids.|
|Pf||Pf/pf||?||Controls distribution of pigmentation of tuber flesh||Requires dominant I (D).|
|Pw||Pw/pw||?||Controls distribution of pigmentation of leaf whorl||Used with diploids; unclear how it applies to tetraploids.|
|R||R/r||2||Red pigmentation (pelargonidin derivatives)||Also previously described as D.|
|Ul||Ul/ul (Pv/pv)||?||Controls distribution of pigmentation of undersides of leaves||Used with diploids; unclear how it applies to tetraploids.|
Someone asked why I included the chromosome number in the chart. That’s a good question, since I never explained it. Genes that are located on the same chromosome are likely to be inherited together. The major color distribution genes are all on chromosome 10 so they may be inherited together. This is known as linkage. It isn’t certain that they will be inherited together because recombination swaps large portions of a chromosome in the process of sexual reproduction, but linkage is always possible when genes are located on the same chromosome.
Purple and Red Pigments
The P locus controls production of petunidin, an anthocyanidin that produces purple coloration. The R locus controls production of pelargonidin, an anthocyanidin that produces red coloration. P is epistatic to R; when both are dominant, purple color is produced rather than red. This is thought to be due to competition between the two genes for a precursor involved in anthocyanidin production. Like anthocyanins, anthocyanidin structure is affected by pH and temperature, at higher pH and/or temperature, color may not be vibrant (or in some cases, not present at all), so coloration is also affected by environment.
Purple and red pigments are distributed to the skin when I is dominant. In the case of homozygous recessive ii, purple and red pigments are not distributed to the skin even if P and/or R are dominant.
Purple and red pigments are distributed to the flesh when Pf is dominant. In the case of homozygous recessive pfpf, diploids do not distribute red or purple pigments to the tuber flesh. Little information is available about the operation of Pf in tetraploids.
There are additional QTLs affecting red and purple flesh color. Loci that influence flesh color have been identified on chromosomes 5, 8, and 9. More detailed information about the operation of these loci has not yet been published as far as I am aware. A more recent study indicated that there may be as many as 27 QTLs influencing flesh color. Amateur breeders probably don’t need to be too concerned about this; the P-R-I complex gives reasonably good predictability. It is enough to be aware that there may be other genes at work if a cross does not conform well to expectations. With a better understanding of all of the involved genes, we could get better predictability of completeness and intensity of pigmentation, but it doesn’t seem like this information will be available in an easily digestible form any time soon.
Orange and Yellow Pigments
Historically, the multiallelic locus Y has been implicated in expression of both orange or yellow flesh. Or (orange flesh) is dominant over Y (yellow flesh), which is dominant over y (white flesh). Or favors production of zeaxanthin over lutein, Y lutein over zeaxanthin, and homozygous yy produces little of either, resulting in white flesh. Yellow flesh has also been found to be a quantitative trait with a number of different QTLs involved that affect intensity. I have searched, but not found any accounting of what occurs when R or P and Or or Y are dominant. From experience, I know that yellow pigments and red or purple pigments can express together, but I don’t know the details. It is also not clear how the Y locus interacts with the various color distribution loci. Again, I know from experience that yellow or orange pigments can sometimes appear in the leaves, but I found no information indicating whether this is controlled by the distribution genes covered above or by different mechanisms. In practice, I have never seen a cross result that made it appear that orange flesh is dominant; instead, orange flesh almost always gives way to less intense yellow flesh.
As noted above, including Or in this locus is now considered dubious. More recent information indicates that orange is developed primarily through the combination of a homozygous recessive pairing of the Zep gene allele 1 (involved in zeaxanthin production) and Chy2 gene allele 3. Very few tetraploid potatoes contain Zep allele 1, which limits the possibility of orange flesh in tetraploids without bringing it from diploids. If this hypothesis holds up, the Zep locus should probably be named Or, yielding a genotype of oror that expresses orange flesh in the presence of allele 3 of Chy2.
The B, I, and F complex controls distribution of pigments to many parts of the plant. These genes probably only distribute purple and red pigment, not orange and yellow, although I have not seen this stated explicitly. B, I, and F comprise a linkage group. They are inherited together.
Ba-d distributes color to the flower abscission zone. This is the joint where the flower connects to the peduncle. There is usually just a small ring right at the joint. In the case of homozygous recessive bb, the joint is the same color as the rest of the inflorescence.
Bb-d distributes color to the tuber eyebrows – the arc shaped structure next to each eye. In the case of homozygous recessive bb, the eyebrow may not be colored when the rest of the skin is.
Bc-d distributes color to the seed spot or embryo spot. This is actually the cotyledonary node, where the hypocotyl is joined to the cotyledons. In the case of homozygous recessive bb, there is no seed spot.
Bd distributes color to the nodes on the stem and possibly also the tuber. In the case of homozygous recessive bb, the result appears to depend on whether the stem has red or blue color, in which case colorless bands can appear at the nodes. This may also extend into cleared spots around the eyes if the tuber skin is colored.
I distributes color to the skin and appears to be dosage dependent. For example, you would expect stronger color in an II diploid than in an Ii. Similarly, in tetraploids, the tubers of a plant with IIII would likely be much more strongly colored than a plant with Iiii. In diploids, I also controls expression of colored flesh (Pf). In the case of recessive ii, tubers will not have colored flesh even if Pf is dominant. Distribution of color to flesh in tetraploids is more complicated and I have not seen it clearly elucidated anywhere.
As noted above, F is a color distribution gene and it acts primarily on the distribution of red and purple pigments to the flowers, as is detailed in the following chart:
|R*ppF*||Pink corolla||Pink because only R is expressed.|
|rrP*F*||Blue corolla||Blue because only P is expressed.|
|R*P*F*||Purple corolla||Purple because P is epistatic to R, but R is still able to contribute some red pigment.|
|R*P*ff||White corolla||White because ff blocks pigment distribution to the flower. The homozygous recessive ff configuration sometimes produces flecked flowers.|
|rrppff||White corolla||White because ff blocks pigment distribution to the flower but also because there is no pigment produced. No possibility for flecked flowers, despite homozygous ff, because there is no pigment to distribute.|
|rrppF*||White corolla||White because there is no pigment to distribute to the flower.|
The chart applies to diploids, which are more straightforward to predict. Tetraploids have four copies of each allele, which can result in some intermediate phenotypes.
Very rarely, potato flowers can also be light yellow. I have found no information about the genetics of this flower color. It is probably too rare to have been studied.
Although anther color is related to overall pigment production, I have not found any clear explanation of its inheritance. It is not included within the F locus. For example, I have several potatoes with red skin and flesh, but white corollas. That presumably puts them in the R*ppppffff genotype, but they also have red anthers, so ffff is clearly not blocking distribution of red to the anthers. Or, perhaps F is affected by dosage and these are something like Ffff. I think that potatoes with red anthers always have red flesh and potatoes with blue anthers always have blue flesh, but, unfortunately, the opposite is not always true. Potatoes with red or blue flesh and white corollas occasionally have yellow anthers. I have not yet seen this in combination with a pigmented abscission zone, so perhaps recessive b genotypes might explain the yellow anthers. That seems rather obvious, so it would probably have been discovered and published by now if it were true.
Most of the foliage color distribution genes, Pd, Pw, and Ul (Pv), have been described only for use with diploids. The same genes must function in tetraploids, but perhaps they do not express in a clear fashion or perhaps they have just not been sufficiently studied. I can say from experience that foliage color seems to be easier to predict in diploids than tetraploids.
Russeting is more a condition of skin structure than color, but still probably fits better in this post than on the future post that I will do on tuber shape and structure. Unfortunately, the inheritance of russeting has not received much study. The only available study was done with diploids and suggests that russeting is controlled by three independently segregating genes. All three genes must be dominant for russeting to appear. The loci have not been named. Inheritance under a three gene system may be very difficult to sort out in tetraploids.
Russeting may also appear as a defect in normally non-russet tubers in calcium poor soils.