Structural inheritance

Prions, the infectious proteins that cause diseases such as scrapie, seen here, propagate by structural inheritance. On left, healthy lymph node tissue; on right, spaces between cells (blue) are filled with (dark red) prion protein.
The centriole, an organelle involved in cell division, is structurally inherited.

Structural inheritance or cortical inheritance is the transmission of an epigenetic trait in a living organism by a self-perpetuating spatial structures. This is in contrast to the transmission of digital information such as is found in DNA sequences, which accounts for the vast majority of known genetic variation.

Examples of structural inheritance include the propagation of prions, the infectious proteins of diseases such as scrapie (in sheep and goats), bovine spongiform encephalopathy ('mad cow disease') and Creutzfeldt–Jakob disease (although the protein-only hypothesis of prion transmission has been considered contentious until recently.)[1] Prions based on heritable protein structure also exist in yeast.[2][3][4] Structural inheritance has also been seen in the orientation of cilia in protozoans such as Paramecium[5] and Tetrahymena,[6] and 'handedness' of the spiral of the cell in Tetrahymena,[6] and shells of snails. Some organelles also have structural inheritance, such as the centriole, and the cell itself (defined by the plasma membrane) may also be an example of structural inheritance. To emphasize the difference of the molecular mechanism of structural inheritance from the canonical Watson-Crick base pairing mechanism of transmission of genetic information, the term 'Epigenetic templating' was introduced.[7][8]

History

Structural inheritance was discovered by Tracy Sonneborn, and other researchers, during his study on protozoa in the late 1930s. Sonneborn demonstrated during his research on Paramecium that the structure of the cortex was not dependent on genes, or the liquid cytoplasm, but in the cortical structure of the surface of the ciliates. Preexisting cell surface structures provided a template that was passed on for many generations.[9]

John R. Preer, Jr., following up on Sonneborn's work, says, "The arrangement of surface structures is inherited, but how is not known, Macronuclei pass on many of their characteristics to new macronuclei, by an unknown and mysterious mechanism."[10]

Other researchers have come to the conclusion that "the phenomena of cortical inheritance (and related nongenic, epigenetic processes) remind us that the fundamental reproductive unit of life is not a nucleic acid molecule, but the remarkably versatile, intact, living cell."[11]

In popular culture

An article in Newsweek mentions research that shows that "Some water fleas sport a spiny helmet that deters predators; others, with identical DNA sequences, have bare heads. What differs between the two is not their genes but their mothers' experiences. If mom had a run-in with predators, her offspring have helmets, an effect one wag called "bite the mother, fight the daughter." If mom lived her life unthreatened, her offspring have no helmets. Same DNA, different traits. Somehow, the experience of the mother, not only her DNA sequences, has been transmitted to her offspring."[12]

Various additional examples of structural inheritance are presented in the recent book Origination of Organismal Form.

References

  1. ↑ Soto C, Castilla J (July 2004). "The controversial protein-only hypothesis of prion propagation". Nat. Med. 10 Suppl (7): S63–7. doi:10.1038/nm1069. PMID 15272271.
  2. ↑ Masison DC, Wickner RB (October 1995). "Prion-inducing domain of yeast Ure2p and protease resistance of Ure2p in prion-containing cells". Science. 270 (5233): 93–5. doi:10.1126/science.270.5233.93. PMID 7569955.
  3. ↑ Tuite MF, Lindquist SL (November 1996). "Maintenance and inheritance of yeast prions". Trends Genet. 12 (11): 467–71. doi:10.1016/0168-9525(96)10045-7. PMID 8973157.
  4. ↑ Serio TR, Cashikar AG, Kowal AS, Sawicki GJ, Lindquist SL (2001). "Self-perpetuating changes in Sup35 protein conformation as a mechanism of heredity in yeast". Biochem. Soc. Symp. (68): 35–43. PMID 11573346.
  5. ↑ Beisson J, Sonneborn TM (February 1965). "Cytoplasmic inheritance of the organization of the cell cortex in paramecium aurelia". Proc. Natl. Acad. Sci. U.S.A. 53 (2): 275–82. doi:10.1073/pnas.53.2.275. PMC 219507Freely accessible. PMID 14294056.
  6. 1 2 Nelsen EM, Frankel J, Jenkins LM (March 1989). "Non-genic inheritance of cellular handedness" (PDF). Development. 105 (3): 447–56. PMID 2612360.
  7. ↑ Viens A, Mechold U, Brouillard F, Gilbert C, Leclerc P, Ogryzko V (July 2006). "Analysis of human histone H2AZ deposition in vivo argues against its direct role in epigenetic templating mechanisms". Mol. Cell. Biol. 26 (14): 5325–35. doi:10.1128/MCB.00584-06. PMC 1592707Freely accessible. PMID 16809769.
  8. ↑ Ogryzko VV (2008). "Erwin Schroedinger, Francis Crick and epigenetic stability". Biol. Direct. 3: 15. doi:10.1186/1745-6150-3-15. PMC 2413215Freely accessible. PMID 18419815.
  9. ↑ Preer JR (March 2006). "Sonneborn and the cytoplasm". Genetics. 172 (3): 1373–7. PMC 1456306Freely accessible. PMID 16554410.
  10. ↑ Preer JR (February 1997). "Whatever happened to paramecium genetics?". Genetics. 145 (2): 217–25. PMC 1207789Freely accessible. PMID 9071578.
  11. ↑ "Cortical Inheritance – Paramecium, Tetrahymena:, Teutophrys, Dileptus, Paramecium:, Pattern Formation: Ciliate Studies and Models – Cell, Cells, Structures, Prion, Genetic, and Information". Science.jrank.org. Retrieved 2011-06-30.
  12. ↑ Sharon BegleyJanuary 17, 2009 (2009-01-17). "Begley: Was Darwin Wrong About Evolution?". Newsweek. Retrieved 2011-06-30.

Further reading

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