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An epigenetic role for maternally inherited piRNAs in transposon silencing. Export

Science, Vol. 322, No. 5906. (2008), pp. 1387-1392.

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balicea's tags for this article

animal-model bio-tech epigenetics evolutionary-genomics evo-tech functional-genome genome-interactome genome-transposon rna systems-biology

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piRNA - piwi-interacting RNA. Small RNAs, expressed in testes. Silencing of transposons. Associated with discrete protein complexes. Maternally-inherited.

Ping-pong cycle - optimizes piRNA population to target active transposon elements (keeps transposons from overtaking genome, overloading cell cycle).

Small RNAs and inheritance (Science podcast - 12/12/08):

  • epigenetics ~ gene expression, RNA regulates epigenetics.
  • piRNAs - specific to animals, control transposons.
  • specificity and recognition components.
  • siRNAs are a mode of transmission.
  • Sperm ~ DNA missile. Egg ~ molecular warehouse. Mother supplies

siRNAs to offspring (wheras sperm get rid of all these).

RISC complex - RNA-induced silencing complex. Multi-protein siRNA complex. Cleaves viral and binds anti-sense RNA (e.g. Dicer).

Drosophila model:

Mother (with transposon A) mates with two groups of fathers:

  • fathers (transposon A)
  • fathers (no transposon A)

If mother lacks transposon A, can only mate with no transposon A fathers (otherwise sterile offspring). Mothers with transposon A can mate with both, as mother is a supplier of piRNAs.

Immunity conferred by piRNAs that can persist over generation

balicea (public note) - 2008-12-17 20:12:05

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In plants and mammals, small RNAs indirectly mediate epigenetic inheritance by specifying cytosine methylation. We found that small RNAs themselves serve as vectors for epigenetic information. Crosses between Drosophila strains that differ in the presence of a particular transposon can produce sterile progeny, a phenomenon called hybrid dysgenesis. This phenotype manifests itself only if the transposon is paternally inherited, suggesting maternal transmission of a factor that maintains fertility. In both P- and I-element-mediated hybrid dysgenesis models, daughters show a markedly different content of Piwi-interacting RNAs (piRNAs) targeting each element, depending on their parents of origin. Such differences persist from fertilization through adulthood. This indicates that maternally deposited piRNAs are important for mounting an effective silencing response and that a lack of maternal piRNA inheritance underlies hybrid dysgenesis.


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