Figure 5.

Hypothetical model of the relationship between W-specific repeat transcription and heterochromatin formation. In black, experimentally confirmed situation; in grey, hypothetical elements. Letter size corresponds to relative strength of the phenomenon. (1) Miracidia do not show sex dimorphism. The W chromosome is euchromatic and repeats are transcribed. Large amounts of Dicer and Argonaute proteins are present [39,40,58]. Dicer could produce small heterochromatic RNA (shRNA) that could bind to Argonauts and could build a RITS (RNA-induced initiation of transcriptional gene silencing) complex similar to those in yeast [42] that initiates heterochromatization around the repeat region of the W chromosome. (2) After infection of the snail host, cercariae are produced. Also, these larvae do not show sex dimorphism. Repeats are still transcribed but transcription of Dicer has decreased [39]. Accumulation of RITS complex around the repeat region progressively leads the loss of its euchromatic character. Finally (3), in dimorphic adults, the repeat region becomes transcriptionally inactive, and heterochromatin is maybe locked by HP1 or related chromatin proteins such as KDM2A [59], or a second histone modification mark is missing [60]. Dicer and Argonaut are less abundant. RITS is no longer necessary. Sexual reproduction occurs during this stage. Recombination is repressed by non-permissive chromatin. Late in germ cell production or during embryogenesis, erasure of chromatin marks occurs (epigenetic reset). The cycle restarts with a euchromatic W chromosome.

Lepesant et al. Genome Biology 2012 13:R14   doi:10.1186/gb-2012-13-2-r14
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