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. Author manuscript; available in PMC: 2012 Jun 9.
Published in final edited form as: Cell. 2011 Nov 23;147(6):1248–1256. doi: 10.1016/j.cell.2011.10.042

Fig.2. Genetic analysis of the transgenerational inheritance of an antiviral response.

Fig.2

Animals of all the genotypes schematically shown in this figure were tested for whether they express GFP after heat shocking adult animals (see Experimental Procedures), as a measure to assess viral silencing; dark animals do not express GFP after heat shock, green animals do. Numbers are shown for the most relevant genotypes. The X-linked FR1gfp transgene is present only when specifically indicated.

(A) Reconstitution of the RNAi machinery re-silences viral production.

(B) The antiviral RNA silencing can pass through the sperm and is independent of the presence of the viral template. Because the FR1gfp array is on the X chromosome, F1 males originating from the cross of male FR1gfp/0 (indicating hemizygosity); rde-1(−/−) with rde-1(−/−) hermaphrodites will not contain the array.

(C) Long-term silenced worms contain a non-chromosomally encoded dominant spreading signal. Crossed animals carry the same genotype in regard to the transgene and rde locus, yet one strain is long-term silenced, while the other has lost its ability to silence. The long-term silenced strain is able to silence the non-silent strain in trans. Viral silencing was always assessed by heat-shock treatment to induce the gfp-tagged viral transcript. If the FR1gfp transgene was not present in a strain, it is not shown in the genotype.