Heterosis, or hybrid vigor, refers to the phenomenon whereby the offspring of different inbred varieties show greater biomass, development speed 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 little. consensus has emerged. With the advent of the genomic era, the means exists to establish a molecular basis for heterosis. Previously, any molecular differences between parents and offspring were attributed to the basis of heterosis Multigenic heterosis has been considered miserably complex, this is how some scientists miss it and that a combinatorial principle will eventually emerge. In this article, we summarize the significant features of heterosis that essentially explains a possible molecular marker.Add figure hereHeterosis in. corn.Say no to. plagiarism. Get a tailor-made essay on "Why Violent Video Games Shouldn't Be Banned"? Get an original essay Classic quantitative genetic explanations for heterosis focus on two concepts (Crow, 1948). The first is “dominance,” which originally meant that heterosis results from complementation in the hybrid of several deleterious alleles that were present in the inbred parental lines by superior alleles of the opposite parent. Over time, this term came to mean the degree 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 each homozygous class. Although these terms have developed a following in each case, both now refer to non-additive situations, of varying degrees. These terms were coined before the molecular concepts of genetics were formulated and are not related to molecular principles. Therefore, they are of limited usefulness for describing the molecular parameters that accompany heterosis. Two extreme models can explain heterosis at the molecular level. In the first model we can imagine that when two different alleles of a different gene are brought together in a hybrid, a combined allelic expression is obtained. IN Model two The combination of different alleles produces an interaction that causes the genetic expression in the hybrid to deviate compared to predictions of the average parent (i.e., by upregulation of many housekeeping genes). The patterns can be considered as the result of gene expression allelic interaction. In 2003 Song and messing provides evidence of altered regulatory effects in hybrids. The challenge in developing the molecular model for heterosis is to create the correct associations between phenotypes and causative molecular events that occur in hybrids. The last century explains heterosis that slightly different and deleterious alleles exist at multiple loci in two inbred lines. In the hybrid produced, all the mutations are integrated, causing the progeny to surpass the parents. This hypothesis has been criticized because if it were the correct explanation then it should promise to produce an inbred line with all superior alleles that shows little or no hybrid vigor, a condition that does not ascend. The counterargument specified that it would be impossible to gather all the best alternatives into a single lineage with so many genes involved in linking the deleterious alleles to the superior allele of the other gene. Although it is accurate that a deleterious allele can become homozygous inseveral inbred lines and that the hybrid would show complementation for these genes. This fact could be reasonable for the hybrid to equal the best of two parents for the effect of the individual gene. Instead, if the complementation of alleles in different genes increases in the phenotype, this will result in heterosis. The molecular question that arises is whether the 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 fundamental principle of heterosis is not limited to simple complementation. Observation Hist. Although inbred lines have improved greatly over the decades, the extent of heterosis has not decreased but has slightly increased. This observation suggests a basis other than simple complementation. East, 1936; Duvick, 1999If heterosis is assumed to be caused by complementation of deleterious alleles and inbred lines have been eradicated, the sum total of heterosis may be reduced. Since heterosis gives the impression of being more resistant to artificial selection than the quality of inbred lines. Especially since the quality of two consanguineous lines does not prompt the quantity of heterosis; this must be intent on a cross. This observation suggests that, rather than replacing alleles of genes that modulate physiological processes important for heterosis, the slight increase in heterosis over the years may have occurred by selecting for alleles at the right 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, varieties of allelic combinations for a gene are possible. In autotetraploids that are hybrids between two inbred lines, Ma is potentially when three or four different alleles are present at various loci. Even in allohexaploid wheat, where three different genomes contribute to the genetic makeup, hybrids between different varieties show heterosis Briggle 1963. Vigor appears to increase as more distinct genomes exist. For simple complementation to explain progressive heterosis, each new stepwise combination of genomes would have to provide increasingly superior alleles to complement preexisting rate-limiting alleles without introducing deleterious alleles at other loci. The probability of this situation occurring is very low. A release from negative dosage effects on vigor by identical alleles could explain progressive heterosis, which is elaborated later. Observation 3 Inbreeding depression in tetraploids of many species proceeds faster than expected based on allele homozygosity. (Randolph, 1942; Alexander and Sonnemaker, 1961; Busbice and Wilsie, 1966; Rice and Dudley, 1974) In a diploid, the sale of a heterozygote (A/B) will produce half of the offspring that are homozygous at one locus and the other half that regenerates the heterozygous condition. In an autotetraploid, selfing of the heterozygote (A/A/B/B) will produce homozygotes (A/A/A/A ​​or B/B/B/B) at any locus in only about 1 in 18 offspring (depending on the degree of binding with the centromere) Furthermore, since the A/A/B/B heterozygotes have been formed again, 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 much different from that in diploids. In some species, theInbreeding depression of tetraploids proceeds faster than at the diploid level. As discovered by Randolph (1942), tetraploid derivatives of maize lines are less vigorous than the diploid parent. Therefore 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 resolution of this finding is to suggest that allelic dosage plays a more important role in tetraploids to generate inbreeding depression than complete homozygosity itself, because allelic dosage changes more rapidly than homozygosity during sale. The increasing number of identical alleles appears to have a negative dosage effect on vigor. If there is any contribution of allele dosage effect in polyploidy heterosis, this understanding is satisfying that most quantitative trait loci show some degree of semi-dominant behavior ( Tanksley, 1993, indicating that quantitative trait is largely influenced by multiple loci showing an allelic dosage effect. Results from aneuploidy studies suggest that quantitative characteristics are influenced by multiple dosage-dependent genes ( Lee et al., 1996 ). these two observations (Guo and Birchler, 1994). What is responsible for such dosage effects? It has been argued that these dosage effects reflect dosage-dependent gene regulatory hierarchies Regulators, mostly genes, reveal some measures of dosage dependence, as target housekeeping genes usually show greater dominant/recessive behavior among 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 yeast diploid loci that tend to have a significant haplo-insufficient effect on growth, they encode products involved in molecular complexes. Regulatory genes in multicellular organisms often function as part of complexes, so if the same rule applies, the regulatory genes will usually show some measure of dosage dependence while the gene encoding metabolic functions will be less likely to show a dosage effect . Empirical observations suggest that most regulatory genes exhibit some type of dosage response (Birchler et al., 2001). Consequently a Quantity will be controlled largely by multiple dosage-dependent regulatory loci. Following 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 show the expected mid-parent value. If heterosis is due to change in gene expression, then what genes are involved and how do these changes compare to the alterations in gene expression that occur in aneuploids, which in most cases are detrimental to vigor? Aneuploidy also causes changes in gene expression typically within a twofold range (Birchler, 1979; Birchler and Newton, 1981; Guo and Birchler, 1994; Auger et al., 2001; Wanous et al., 2003). These changes can result from structural gene dosage effects, but more often result from transaction effects that modulate the expression of most of the genome (Birchler et al., 2001; Matzke et al.,