Dominance and recessivity
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Dominance and recessivity are relations between two alleles of a gene, seen in a plant that carries one copy of each, a heterozygote. An allele is dominant for a character when the heterozygote matches the plant with two copies of it. It is recessive when its effect is hidden in the heterozygote and shows only in plants with two copies. With partial dominance the heterozygote falls between the two homozygotes but nearer one of them. With no dominance it falls midway. A heterozygote that lies beyond both homozygotes shows overdominance.[1][2]
Single-locus cases in Cannabis include flowering and chemotype. Flowering regardless of day length, the habit of autoflowering cultivars, is recessive when it comes from the locus Autoflower1 and dominant when it comes from a second locus, Autoflower2, found in the hemp cultivar FINOLA.[3][4] The ratio of THC to CBD is intermediate in plants that carry alleles for both, an inheritance that de Meijer and colleagues called codominant.[5][6] A rare recessive allele sits almost entirely in heterozygotes, where it has no effect, so selection changes its frequency only slowly; inbreeding brings such alleles to light.[7][8]
The heterozygote between its parents
Plant breeders place the three genotypes at a locus with two alleles, A and a, on one scale. The homozygote AA takes the value +a and the homozygote aa the value −a. Their midpoint is zero. The heterozygote Aa takes the value d, which measures dominance. With no dominance d is zero. When A is dominant or partially dominant, d lies on the side of AA; when a is, it lies on the side of aa. Dominance is complete when d equals +a or −a. Overdominance places d beyond either homozygote.[2]
The words dominant and recessive come from Gregor Mendel's paper on hybrids of the pea. Mendel called dominant the characters that pass into the hybrid wholly or nearly unchanged. Those that become latent in it he called recessive. He chose "recessive" because such characters recede or disappear in the hybrid and then reappear unchanged among its progeny. In each of the seven pairs of characters he crossed, the hybrid resembled one parent so closely that the other parent's character escaped notice. The hybrid was the same whichever parent gave the pollen. In his earlier crosses of ornamental plants, characters such as the form and size of the leaves and their hairiness had almost always given an intermediate hybrid.[1]
Etienne de Meijer and colleagues crossed inbred plants of pure CBD and pure THC chemotype. Every F1 plant had a mixed chemotype. The F2 progenies segregated pure CBD, mixed and pure THC plants in a 1:2:1 ratio. The authors proposed a locus, B, with two codominant alleles, BD and BT. They suggested that the alleles code for two forms of one synthase that convert a common precursor into CBD or into THC.[5] Jonathan Wenger and colleagues tied the three classes to functional and non-functional alleles of CBDA synthase. Plants with two functional copies have mainly CBD, plants with two non-functional copies mainly THC and heterozygotes an intermediate ratio. The genotypes in a test cross among feral plants fitted codominant Mendelian inheritance. The same paper also calls the pattern incomplete dominance.[6] The two synthase genes lie at separate but closely linked loci, a linkage that Grassa and colleagues took to explain their inheritance as a single locus.[9] The arrangement of the locus is described under Genetic traits.
Genetic markers are classed in the same way. A codominant marker shows both alleles of a heterozygote, so heterozygotes can be told from homozygotes; microsatellites and allozymes are codominant markers.[10] The marker that de Meijer and colleagues developed for the B locus is tightly linked to chemotype and codominant.[5]
Day-neutral flowering
Under long days of 16 hours, 28 of 88 plants in one population and 24 of 88 in another flowered, close to the quarter expected when a recessive allele segregates in the second generation of a cross. Jacob Toth and colleagues named the locus Autoflower1. Plants heterozygous at it did not flower under continuous light. In a field trial in 2021, however, heterozygotes were intermediate between the two homozygotes in the date of flowering, in height and in fresh biomass. Toth and colleagues describe Autoflower1 as recessive with respect to insensitivity to day length. In a complementation test they crossed Le Crème plants homozygous for Autoflower1 with the Canadian grain hemp Picolo, which also flowers under continuous light but gave a different marker call at the locus. Every F1 plant flowered under long days. Female Le Crème plants flowered after four weeks, female Picolo and F1 plants after seven. The female F1 plants resembled Picolo in form. The authors judged the test inconclusive.[3]
The day-neutral flowering of FINOLA and Picolo maps to a different locus, Autoflower2. It lies on chromosome 8, Autoflower1 on chromosome 1. Caroline Dowling and colleagues found that second-generation plants with one or two copies of the FINOLA allele of an FT-like gene, CsFT1, did not differ in flowering time. They judged Autoflower2 dominant with respect to flowering under continuous light. They crossed a plant of the cultivar Le Crème, homozygous for the day-neutral allele at Autoflower1, with plants of the cultivar Picolo, homozygous for the FINOLA-type allele at Autoflower2. In the offspring, 98.9 per cent of the plants that carried at least one day-neutral allele at Autoflower2 or two at Autoflower1 flowered under continuous light.[4] The response of cannabis to day length is described under Photoperiod response.
Why mutant alleles are often recessive
Rare visible mutants are recessive to the wild type far more often than they are dominant. R.A. Fisher explained this in 1928 and 1930 by selection at other loci. Because a rare mutant occurs almost only in heterozygotes, modifier alleles that raised the fitness of the heterozygote would be favoured far more than those acting on the homozygote. The mutant would then evolve towards complete recessiveness. Sewall Wright replied in 1929 that selection on such modifiers was far too weak, given how rare the mutants are, to prevail against genetic drift. J.B.S. Haldane and Muller sided with Wright and gave more directly physiological reasons for the recessiveness of deleterious mutants.[11] A review of the evidence by Brian Charlesworth in 1979 came down on the side of Wright and Haldane.[12]
Mutations can be classed by what they do to the gene's product. A loss-of-function mutation reduces or removes the function of a protein and is often recessive, since one working copy of the gene can make up for the loss. A gain-of-function mutation gives a new or stronger function and is often dominant, since the change shows even beside a normal copy. A dominant-negative mutation makes a protein that interferes with the normal one. It is typically dominant because it acts on the function of both alleles.[13]
The candidate genes for Autoflower2 included the FT-like gene CsFT1 and relatives of two repressors of flowering, ELF9 and AGO5. A loss-of-function mutation of ELF9 is recessive in Arabidopsis. So are loss-of-function mutations of the AGO5 homologue in soybean. Autoflower2 is dominant. Dowling and colleagues therefore took CsFT1 to be the more likely candidate.[4] In the chemotype, by contrast, the effect of a non-functional allele of CBDA synthase does not disappear in the heterozygote: plants with one functional and one non-functional copy have intermediate ratios.[6]
Recessive alleles in populations
A rare allele occurs mostly in heterozygotes. When it is recessive, carriers and non-carriers differ in fitness only through the few homozygotes, so selection changes its frequency very slowly, whether the allele is favoured or harmful.[7] Severely deleterious rare mutants tend to be recessive. Inbreeding raises the share of plants homozygous for them.[8] The resulting inbreeding depression in cannabis is described under outcrossing, with its two explanations by dominance and by overdominance. Overdominance is sometimes confused with heterosis, the advantage of a cross between populations over its parents, which may or may not be due to overdominance.[14]
V.A. Serkov and L.V. Klimova, reviewing earlier work on inbred hemp, write that hemp cultivars are complex populations of heterozygous plants and that forced self-pollination brings out useful characters held in a recessive state. They state that monoecy and the absence of THC are recessive in hemp. They cite R.I. Kaplunova's finding that valuable recessive characters, monoecy above all, appear in the phenotype once they become homozygous. In L.M. Gorshkova's inbred progenies of the cultivar YuSO-29, selected against cannabinoids, the frequency of the recessive allele rose to 0.994 by the 16th generation. Plants with branched or fasciated stems and with pinnately incised or whorled leaves split out in inbred lines and are due to single recessive genes. These forms are rare under free cross-pollination and much more frequent in inbred lines. Haploid plants show all their recessive genes within one generation. In hemp, spontaneous haploids can reach 3 per cent.[15] The leaf forms are described under Leaf morphology.
Many cultivars on the market are heterozygous for Autoflower1. Toth and colleagues found populations sold as cultivars that segregated for day-neutral flowering. They suggested that the breeders had used parents heterozygous at the locus.[3]
Dominance in quantitative variation
For a quantitative trait, the genetic value of a plant can be split into two parts. The average effects of its alleles taken one at a time sum to its breeding value. The interactions between the two copies at each locus are called dominance deviations. Their variances are the additive variance and the dominance variance, which with the environmental variance make up the variance of the phenotype. At a locus with no dominance there is no dominance variance.[16] Narrow-sense heritability counts the additive variance only. The additive variance and the total variance of the phenotype are all that is needed to predict the response to selection, as in mass selection.[17][18]
When a completely dominant allele has a frequency of 0.1, dominance accounts for about 5 per cent of the genetic variance at the locus. At a frequency of 0.5 it accounts for a third, at 0.9 for about 82 per cent. A rare dominant allele is seldom seen in homozygotes, so its dominance is hard to detect. Loci dominant in opposite directions do not cancel, since each adds its own dominance variance. The amount of dominance variance is therefore a poor guide to the kind of gene action at the loci behind that variance.[16]
See also
References
- ↑ 1.0 1.1 Abbott, S.; Fairbanks, D.J. (2016). "Experiments on Plant Hybrids by Gregor Mendel". Genetics. 204 (2): 407–422. doi:10.1534/genetics.116.195198. PMC 5068836.
- ↑ 2.0 2.1 Beavis, W.; Lamkey, K.; Espinosa, K.; Mahama, A.A.; Suza, W. (2023). "Gene Effects". In Suza, W.; Lamkey, K. (eds.). Quantitative Genetics for Plant Breeding. Iowa State University Digital Press. doi:10.31274/isdup.2023.146.
- ↑ 3.0 3.1 3.2 Toth, J.A.; Stack, G.M.; Carlson, C.H.; Smart, L.B. (2022). "Identification and mapping of major-effect flowering time loci Autoflower1 and Early1 in Cannabis sativa L." Frontiers in Plant Science. 13 991680. doi:10.3389/fpls.2022.991680.
- ↑ 4.0 4.1 4.2 Dowling, C.A.; Shi, J.; Toth, J.A.; Quade, M.A.; Smart, L.B.; et al. (2024). "A FLOWERING LOCUS T ortholog is associated with photoperiod-insensitive flowering in hemp (Cannabis sativa L.)". The Plant Journal. 119 (1): 383–403. doi:10.1111/tpj.16769.
- ↑ 5.0 5.1 5.2 de Meijer, E.P.M.; Bagatta, M.; Carboni, A.; Crucitti, P.; Moliterni, V.M.C.; Ranalli, P.; Mandolino, G. (2003). "The inheritance of chemical phenotype in Cannabis sativa L.". Genetics. 163 (1): 335–346. doi:10.1093/genetics/163.1.335.
- ↑ 6.0 6.1 6.2 Wenger, J.P.; Dabney, C.J.; ElSohly, M.A.; Chandra, S.; Radwan, M.M.; Majumdar, C.G.; Weiblen, G.D. (2020). "Validating a predictive model of cannabinoid inheritance with feral, clinical, and industrial Cannabis sativa". American Journal of Botany. 107 (10): 1423–1432. doi:10.1002/ajb2.1550. PMC 7702092.
- ↑ 7.0 7.1 Felsenstein, J. (December 2019). Theoretical evolutionary genetics. Seattle: Department of Genome Sciences, University of Washington. p. 80.
- ↑ 8.0 8.1 Felsenstein, J. (December 2019). Theoretical evolutionary genetics. Seattle: Department of Genome Sciences, University of Washington. pp. 242–244.
- ↑ Grassa, C.J.; Weiblen, G.D.; Wenger, J.P.; Dabney, C.; et al. (2021). "A new Cannabis genome assembly associates elevated cannabidiol (CBD) with hemp introgressed into marijuana". New Phytologist. 230 (4): 1665–1679. doi:10.1111/nph.17243. PMC 8248131.
- ↑ Davinack, D. (2024). Molecular Ecology & Evolution: An Introduction. Norton, Massachusetts: Wheaton College. pp. 153–154.
- ↑ Felsenstein, J. (December 2019). Theoretical evolutionary genetics. Seattle: Department of Genome Sciences, University of Washington. p. 165.
- ↑ Felsenstein, J. (December 2019). Theoretical evolutionary genetics. Seattle: Department of Genome Sciences, University of Washington. p. 385.
- ↑ Davinack, D. (2024). Molecular Ecology & Evolution: An Introduction. Norton, Massachusetts: Wheaton College. pp. 29–30.
- ↑ Felsenstein, J. (December 2019). Theoretical evolutionary genetics. Seattle: Department of Genome Sciences, University of Washington. p. 85.
- ↑ Serkov, V.A.; Klimova, L.V. (2016). "Sozdanie i izuchenie samoopylennykh linii dlya prakticheskoi selektsii nenarkoticheskoi konopli posevnoi" [Creation and study of self-pollinated lines for the practical breeding of non-narcotic seed hemp]. Niva Povolzh'ya (in русский) (2 (39)): 52–60.
- ↑ 16.0 16.1 Felsenstein, J. (December 2019). Theoretical evolutionary genetics. Seattle: Department of Genome Sciences, University of Washington. pp. 423–425.
- ↑ Felsenstein, J. (December 2019). Theoretical evolutionary genetics. Seattle: Department of Genome Sciences, University of Washington. pp. 429–430.
- ↑ Felsenstein, J. (December 2019). Theoretical evolutionary genetics. Seattle: Department of Genome Sciences, University of Washington. pp. 434–435.