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The hypothesized transition from RNA to proteins to DNA

The RNP world is a hypothesized intermediate period in the origin of life characterized by the existence of ribonucleoproteins.[1] The period followed the hypothesized RNA world and ended with the formation of DNA and contemporary proteins.[2] In the RNP world, RNA molecules began to synthesize peptides. These would eventually become proteins which have since assumed most of the diverse functions RNA performed previously. This transition paved the way for DNA to replace RNA as the primary store of genetic information, leading to life as we know it.[3]


Principle of concept

Thomas Cech, in 2009, proposed the existence of the RNP world after his observation of apparent differences in the composition of catalysts in the two most fundamental processes that maintain and express genetic systems. The maintenance process, DNA replication and transcription, is accomplished purely by protein polymerases. The gene expression process, mRNA splicing and protein synthesis, is catalyzed by RNP complexes (the spliceosome and ribosome).

The difference between how these processes catalyze can be reconciled with the RNA world theory. As an older molecule than DNA, RNA had a hybrid RNA-protein-based maintenance system. Our current DNA world could have resulted from the gradual replacement of RNA catalysis machines with proteins. In this view, ribonucleoproteins and nucleotide-based cofactors are relics of an intermediary era, the RNP world.[3]

See also

References

  1. ^ Cech, Thomas R. (July 2012). "The RNA Worlds in Context". Cold Spring Harbor Perspectives in Biology. 4 (7): a006742. doi:10.1101/cshperspect.a006742. ISSN 1943-0264. PMC 3385955. PMID 21441585.
  2. ^ Schimmel, Paul (March 2011). "The RNP bridge between two worlds". Nature Reviews Molecular Cell Biology. 12 (3): 135. doi:10.1038/nrm3061. ISSN 1471-0080. PMID 21285979. S2CID 21589855.
  3. ^ a b Cech, Thomas R. (2009-02-20). "Crawling Out of the RNA World". Cell. 136 (4): 599–602. doi:10.1016/j.cell.2009.02.002. ISSN 0092-8674. PMID 19239881. S2CID 13933577.