Hybrid vigour

difference in a quantitative trait between heterozygous and homozygous genotypes

Hybrid vigour (or hybrid vigor) is the improved activity and survival of hybrid offspring. The technical term in genetics is heterosis.

Inbreeding in a normal population leads to the offspring getting worse, less fit, less fertile and usually not living as long as the parents. The opposite, outbreeding, leads to fit, healthy, fertile offspring. This effect has been known for a long time. Animal breeders have known it since the 18th century, and Darwin investigated it in detail with plants.[1][2]

On the other hand, when two parents are from widely different populations, such as different subspecies, this usually does not apply. In that case it is more usual for the hybrids to have lower fitness. Mules are usually not fertile, and that automatically makes them of lower fitness, as that term is used in biology. They are very hardy animals, but they leave few offspring. The puzzle for scientists has been to explain these facts.

Genetic theories


When a population is small or inbred, it tends to lose genetic diversity. The loss of fitness is due to loss of genetic diversity. Inbred strains tend to be homozygous for recessive alleles. Recessive alleles tend to be mildly harmful. Heterosis or hybrid vigor, on the other hand, is the tendency of outbred strains to exceed both inbred parents in fitness.

In the early 20th century, after Mendel's laws came to be understood and accepted, two explanations were proposed.[3]

Genetic basis of heterosis. Dominance hypothesis. Scenario A. Fewer genes are under-expressed in the homozygous individual. Gene expression in the offspring is equal to the expression of the fittest parent. Overdominance hypothesis. Scenario B. Over-expression of certain genes in the heterozygous offspring. (The size of the circle depicts the expression level of gene A)
  • Dominance hypothesis. Undesirable recessive alleles from one parent are suppressed by dominant alleles from the other. Inbred strains lose genetic diversity, because they become homozygous at many loci.
  • Overdominance hypothesis. Certain combinations of alleles that can be obtained by crossing two inbred strains are advantageous in the heterozygote. Cases such as sickle-cell anaemia show this at one gene locus, and overdominance is explained by this happening at many loci.

Present status


At present, the first idea seems to fit the facts best. "The current view ... is that the dominance hypothesis is the major explanation of inbreeding decline and the high yield of hybrids".[4]

An epigenetic effect heterosis has been found in plants,[5] and also in animals.[6] MicroRNAs (miRNAs) are small non-coding RNAs which repress the translation of messenger RNAs (mRNAs) or degrade mRNAs.[7] The miRNAs may also have an effect on hybrid vigour.[8]


  1. Ashby E. 1948. Hybrid vigour. In New Biology 4, 9–25.
  2. Darwin C.D. 1876. The effects of cross and self fertilisation in the vegetable kingdom. London: Murray.
  3. Crow, James F. (1948). "Alternative hypotheses of hybrid vigor". Genetics. 33 (5): 477–487. doi:10.1093/genetics/33.5.477. PMC 1209419. PMID 17247292.
  4. Crow, James F. (1998). "90 years ago: the beginning of hybrid maize". Genetics. 148 (3): 923–928. doi:10.1093/genetics/148.3.923. PMC 1460037. PMID 9539413.
  5. Baranwal V.K.; et al. (November 2012). "Heterosis: emerging ideas about hybrid vigour". J. Exp. Bot. 63 (18): 6309–14. doi:10.1093/jxb/ers291. PMID 23095992.[permanent dead link]
  6. Han Z.; et al. (2008). "Hybrid vigor and transgenerational epigenetic effects on early mouse embryo phenotype". Biol. Reprod. 79 (4): 638–48. doi:10.1095/biolreprod.108.069096. PMC 2844494. PMID 18562704. Archived from the original on 2013-04-14. Retrieved 2015-07-14.
  7. Zhou Y.; et al. (2007). "Inter- and intra-combinatorial regulation by transcription factors and microRNAs". BMC Genomics. 8: 396. doi:10.1186/1471-2164-8-396. PMC 2206040. PMID 17971223.
  8. Ni Z.; et al. (2009). "Altered circadian rhythms regulate growth vigour in hybrids and allopolyploids". Nature. 457 (7227): 327–31. Bibcode:2009Natur.457..327N. doi:10.1038/nature07523. PMC 2679702. PMID 19029881.