Heterosis, or hybrid vigor, refers to the phenomenon where the progeny of various inbred varieties exhibit greater biomass, developmental rate and fertility than the better of the two parents (Add the figure of Brassica napus heterosis This phenomenon has been widely exploited in agricultural production and has been a powerful force in plant evolution. The genetic basis was postulated almost a century ago (Shull, 1908; Bruce, 1910; Jones, 1917), but there is little consensus With the advent of the genomic era, the tool to establish a molecular basis for heterosis previously exists. descent was attributed to the basis of heterosis was considered miserably complex, so some scientists abandoned it and eventually a principle of combination will emerge. In this article, we summarize the significant features. of heterosis that is essentially explained by a possible molecular marker.Add a figure hereHeterosis in corn.Say no to. plagiarism. Get a tailor-made essay on “Why Violent Video Games Should Not Be Banned”? Get an original essay Classic quantitative genetic explanations of heterosis focus on two concepts (Crow, 1948). The first is “dominance,” which originally meant that heterosis results from the complementation in the hybrid of different deleterious alleles present in the inbred parental lines by superior alleles from the opposite parent. Over time, this term came to refer to the extent to which the heterozygous genotype behaves differently from the average of the two homozygous classes. The second historical explanation for heterosis is "overdominance", which refers to the idea that allelic interactions occur in the hybrid such that the heterozygous class performs better than either class homozygous. Although these terms have developed a sequence in each case, they now both refer to non-additive situations, to different degrees. These terms were coined before the formulation of the molecular concepts of genetics and are not related to molecular principles. Therefore, their usefulness is reduced for describing the molecular parameters that accompany heterosis. Two extreme models can explain heterosis at their molecular level. In model one, we can imagine that when two different alleles of a different gene are brought together in a hybrid, this leads to a combined allelic expression. In model two, the combination of different alleles produces an interaction that causes a deviation of gene expression in the hybrid relative to the predictions of the intermediate parent (i.e. by upregulation of many housekeeping genes). Patterns can be seen as the result of gene expression. allelic interaction. In 2003, Song and Messing provided evidence of altered regulatory effects in hybrids. The challenge in developing a molecular model for heterosis is to establish the correct associations between phenotypes and the causal molecular event that occurs in hybrids. The last century explains heterosis by the fact that slightly different and deleterious alleles exist at several loci in two inbred lines. In the hybrid produced, all mutations are completed, causing the offspring to outgrow the parents. This hypothesis has been criticized that if it is the correct explanation, then it should promise to produce an inbred line possessing all the superior alleles and showing minimal or no hybrid vigor, a condition which does not ascend. THEcounterargument specified that it would be impossible to collect all the best alternatives into a single lineage with so many genes involved in linking the deleterious alleles with the superior allele of the other gene. Although it is true that a deleterious allele can become homozygous in different inbred lines and the hybrid would show complementation for these genes. This fact could be reasonable for the hybrid to be equivalent to the best of the two parents for the effect of the individual gene. Instead, if the complementation of alleles in different genes increased in the phenotype, this would result in heterosis. The molecular question that arises is whether simple complementation of slightly different and deleterious alleles causes a growth response that can lead to heterosis. However, several observations related to heterosis suggest that the basic principle of heterosis is not limited to simple complementation.Observation Ist. Although inbred lines have improved significantly over the decades, the extent of heterosis has not decreased but increased slightly. This observation suggests a basis other than simple complementation. East, 1936; Duvick, 1999. If heterosis is believed to be caused by complementation of deleterious alleles and inbred lines have been eradicated, the sum total of heterosis could be diminished. As heterosis gives the appearance of being more resistant to artificial selection than the quality of inbred lines. Furthermore, the quality of two inbred lines does not influence the amount of heterosis; this must be the intention of a cross. This observation suggests that instead of replacing alleles of genes that modulate physiological processes important for heterosis, the slight increase in heterosis over the years could have occurred by selecting alleles at the correct set of loci that constitute the best combination in hybrids to cause heterosis. 2nd. Progressive heterosis in tetraploids argues against simple complementation (Levings et al., 1967; Mok and Peloquin, 1975; Groose et al., 1989; Bingham et al., 1994). Two alleles of a gene can occur in an individual at the diploid level. However, at a higher ploidy level, various allelic combinations are possible for a gene. In autotetraploid hybrids between two inbred lines, but this is potentially the case when there are three or four different alleles present at different loci. Also in allohexaploid wheat, where three different genomes contribute to the genetic makeup, hybrids between various varieties exhibit heterosis Briggle 1963. It appears that vigor increases as there are a greater number of distinct genomes. For simple complementation to explain progressive heterosis, each new progressive combination of genomes would need to provide increasingly superior alleles to complement pre-existing limiting alleles without introducing deleterious alleles at other loci. The probability of this situation occurring is very low. A release of negative dosage effects on vigor by identical alleles could explain progressive heterosis, which is elaborated in more detail below. Observation 3 Inbreeding depression in tetraploids of many species proceeds more rapidly than expected based on allele homozygosity. 1961; Busbice and Wilsie, 1966; Rice and Dudley, 1974) In a diploid, the sale of a heterozygote (A/B) will produce half the offspring homozygous at one locus and the other half which will regenerate the heterozygous state. In an autotetraploid, self-fertilization of heterozygotes (A/A/B/B) will produce homozygotes (A/A/A/A ​​or B/B/B/B) at any locus at only ∼ 1 of 18descendants (depending on the degree of centromere binding) In addition, as the A/A/B/B heterozygotes are formed again, the A/A/A/B and B/B/B/A heterozygotes are present in the population. Regardless of this difference in the rate of progression to heterozygosity, the trajectory of inbreeding depression in tetraploids is often faster than expected and not significantly different from that of diploids. In some species, inbreeding depression in tetraploids proceeds more rapidly than at the diploid level. As Randolph (1942) discovered, tetraploid derivatives of corn lines are less vigorous than the diploid parent. Thus, in this species, the end product of inbreeding depression in tetraploids is lower than in diploids, although the genotype is identical (but differs in dosage). One solution to this finding is to suggest that allelic dosage plays a greater role in tetraploids in generating inbreeding depression than does the complete homozygote itself, because allelic dosage shifts faster than homozygosity over the course of the sale. The increasing number of identical alleles appears to have a negative dosage effect on vigor. If there is a contribution of the allele dosage effect in polyploid heterosis, this understanding is satisfactory because the majority of quantitative trait loci exhibit some degree of semi-dominant behavior (Tanksley, 1993, indicating that the trait quantitative is largely affected by several loci exhibiting an allelic dosage effect Results from aneuploidy studies suggest that quantitative traits are affected by several dosage-dependent genes (Lee et al., 1996). These two observations (Guo and Birchler, 1994) What is responsible for such dosage effects? These dosage effects have been estimated to reflect dosage-dependent hierarchies of genetic regulation (Birchler et al., 2001). Regulatory genes, for the most part, reveal some measure of dosage dependence, as target housekeeping genes generally exhibit greater dominant/recessive behavior between allelic alternatives (Birchler and Auger, 2003). A possible explanation for this partial dichotomy comes from an analysis of dosage-sensitive genes in yeast (Papp et al., 2003). In diploid yeast loci that tend to have a significant haploinsufficient effect on growth encode products involved in molecular complexes. Regulatory genes in multicellular organisms often function as part of complexes. Thus, if the same rule applies, regulatory genes will generally exhibit some measure of dosage dependence, while genes that encode metabolic functions will be less likely to exhibit a dosage effect. Empirical observations suggest that most regulatory genes exhibit some sort of dose response (Birchler et al., 2001). As a result, a quantitative will be controlled largely by multiple dosage-dependent regulatory loci. In this context, one may be led to the idea that heterosis is the result of the presence of different alleles at loci that contribute to the regulatory hierarchies that control quantitative traits. Gene expression in inbreds and hybrids suggests a change in gene regulation in hybrids. Romagnoli et al. (1990), Leonardi et al. (1991), (Osborn et al., 2003) and Song and Messing (2003), their study suggests that the expression of many genes does not present the expected mid-parental value. If heterosis is due to a change in gene expression, then which genes are involved and how these changes occur