Inheritance of acquired characteristics

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"Acquired characteristics" redirects here. For non-hereditary changes, see Acquired characteristic.
Jean-Baptiste Lamarck

The inheritance of acquired characteristics is a hypothesis that physiological changes acquired over the life of an organism (such as the enlargement of a muscle through repeated use) may be transmitted to offspring.[1] It is also commonly referred to as the theory of adaptation equated with the evolutionary theory of French naturalist Jean-Baptiste Lamarck known as Lamarckism.


The idea was proposed in ancient times by Hippocrates and Aristotle, and was commonly accepted near to Lamarck's time. Erasmus Darwin had described the inheritance of acquired characters in his Zoonomia, 1794. According to historian of science Conway Zirkle:

Lamarck was neither the first nor the most distinguished biologist to believe in the inheritance of acquired characters. He merely endorsed a belief which had been generally accepted for at least 2,200 years before his time and used it to explain how evolution could have taken place. The inheritance of acquired characters had been accepted previously by Hippocrates, Aristotle, Galen (?), Roger Bacon, Jerome Cardan, Levinus Lemnius, John Ray, Michael Adanson, Jo. Fried. Blumenbach and Erasmus Darwin among others.[2]

Lamarck published his theory in 1809, the year Darwin was born. He noticed several lines of descent by comparing current species with fossil forms. He noticed that the younger the fossils were, the more alike they were to modern species. Two ideas were incorporated in Lamarck’s theory. The first was the theory of use and disuse; the idea that body parts used more often become stronger and larger, while parts not used slowly waste away and disappear. The second idea was the inheritance of acquired characteristics theory, the concept that modifications that occur during an organism's lifetime are passed on to its offspring. His example was the giraffe. He believed that the long neck of the giraffe resulted from the ancestors of giraffes stretching their necks longer and longer while trying to reach the highest branches of the trees.[3] Comte de Buffon, before Lamarck, proposed ideas about evolution involving the concept, and even Charles Darwin, after Lamarck, developed his own theory of inheritance of acquired characters, pangenesis. The basic concept of inheritance of acquired characters was finally widely rejected in the early 20th century.

In the 1920s, Harvard University researcher William McDougall studied the abilities of rats to correctly solve mazes. His reports claimed that offspring of rats that had learned the maze were able to run it faster. In his data, the first rats would get it wrong 165 times before being able to run it perfectly each time, but after a few generations, it was down to 20. McDougall attributed this to some sort of Lamarckian evolutionary process. However McDougall's results have never been replicated by other experimenters, and have been criticised for having several methodological problems and poor record-keeping.[4][5]

During the rule of Joseph Stalin in the USSR in the 1930s, the theory of inheritance of acquired characteristics was central to the dogma put forth by Trofim Lysenko, president of the Soviet Academy of Agricultural Sciences. Lysenkoism was advanced primarily in service to Soviet agriculture, always resulting in dismal failure.


The idea that germline cells contain information that passes to each generation unaffected by experience and independent of the somatic (body) cells, came to be referred to as the Weismann barrier, and is frequently quoted as putting a final end to theory of inheritance of acquired characteristics.

Weismann conducted the experiment of removing the tails of 68 white mice, repeatedly over 5 generations, and reporting that no mice were born in consequence without a tail or even with a shorter tail. He stated that "901 young were produced by five generations of artificially mutilated parents, and yet there was not a single example of a rudimentary tail or of any other abnormality in this organ."[6]

Transgenerational epigenetic inheritance[edit]

For more details on this topic, see transgenerational epigenetics

Recently, researchers have reexamined this concept in light of discoveries in epigenetics and transgenerational epigenetics. The study of Heijmans et al. (2008) studied people born during the Dutch Hunger Winter in 1944–1945. Adults who were conceived during the famine had distinct epigenetic marks that their siblings born before or after the famine did not. These marks reduced the production of insulin-like growth factor 2 (IGF2), affected the children's growth. While transgenerational epigenetic inheritance could have occurred, the findings could also be explained by in utero modifications due to famine, rather than germline inheritance.[7] Further, environmental stress in experimental mice that caused aggressive behavior in males caused the same behavior in their offspring, who had DNA methylation patterns changes for particular genes.[8]

The mechanism of transgenerational epigenetic inheritance appears to involve long noncoding RNAs (lncRNAs), which are transcripts generally expressed from regions that are thought not to code for proteins. Some lncRNAs bind to transcripts from protein coding genes. Associated chromatin-remodeling proteins than modify local chromatin and DNA through mechanisms such as DNA methylation, suppressing gene expression. Kevin Morris's 2012 article in The Scientist[9] discusses heritability of epigenetic changes in depth.

See also[edit]


  1. ^ Martin, Elizabeth; Hine, Robert. (2015). A Dictionary of Biology. Oxford University Press. p. 6. ISBN 978-0-19-871437-8
  2. ^ Zirkle, Conway. (1935). The Inheritance of Acquired Characters and the Provisional Hypothesis of Pangenesis. The American Naturalist 69: 417-445.
  3. ^ Campbell, Neil; Reece, Jane (March 2011) [2002], "22", Biology (Sixth ed.), Benjamin Cummings, p. 431 
  4. ^ Agar, WE; Drummond, FH; Tiegs, OW; Gunson, MM. "Fourth (final) report on a test of McDougall's Lamarckian experiment on the training of rats" (PDF). 1954 31 (3): 307–21. 
  5. ^ Crew, F. A. E. (1936). "A repetition oe modougall’s lamarckian experiment". Journal of Genetics 33 (1): 61–102. doi:10.1007/BF03027604. 
  6. ^ Weismann, August. (1889).Essays Upon Heredity. Clarendon Press, Oxford.
  7. ^ Heijmans, B. T.; Tobi, E. W.; Stein, A. D.; Putter, H.; Blauw, G. J.; Susser, E. S.; Slagboom, P. E.; Lumey, L. H. (2008). "Persistent epigenetic differences associated with prenatal exposure to famine in humans". Proceedings of the National Academy of Sciences 105 (44): 17046–9. Bibcode:2008PNAS..10517046H. doi:10.1073/pnas.0806560105. JSTOR 25465222. PMC 2579375. PMID 18955703. 
  8. ^ Franklin, Tamara B.; Mansuy, Isabelle M. (2010). "Epigenetic inheritance in mammals: Evidence for the impact of adverse environmental effects". Neurobiology of Disease 39 (1): 61–5. doi:10.1016/j.nbd.2009.11.012. PMID 19931614. 
  9. ^ Morris, Kevin V. (October 1, 2012). "Lamarck and the Missing Lnc". The Scientist. 


  • Campbell, Neil; Reece, Jane (March 2011) [2002], "22", Biology (Sixth ed.), Benjamin Cummings, p. 431