Skip to main content
Fig. 5 | Genome Biology

Fig. 5

From: Transposable elements in the mammalian embryo: pioneers surviving through stealth and service

Fig. 5

Proposed models of de novo endogenous retrovirus (ERV) silencing in embryonic stem cells. a To initiate silencing, the Krüppel-associated box (KRAB) zinc finger protein (Zfp) Zfp809 interacts with the proline primer binding site (PBS Pro) of some ERV families (e.g., Moloney murine leukemia virus) [85] whereas other KRAB-Zfps bind to a short heterochromatin-inducing (SHIN) sequence found in intracisternal A-type particle retrotransposons and other ERV families [93]. Subsequently, Trim28 is recruited by the Zfps [74, 86], assisted by binding of YY1 to the long terminal repeat (LTR) and Trim28 [92]. Interaction with HP1 and sumolyation by Sumo2 are thought to contribute to transcriptional repression mediated by Trim28 [72, 86, 89]. Eset also interacts with Trim28 and enables trimethylation of H3K9 and H4K20 [73]. The histone chaperone Chaf1a, aided by Asf1a/b, marks proviral DNA for silencing by depositing histones H3 and H4 and interacts with Eset [72]. b Conflicting models of ERV silencing by H3.3 deposition. The Atrx–Daxx complex is suggested to play an important role in SHIN-mediated silencing, which is H3.3-independent. Here, Atrx is thought to promote ERV heterochromatin inaccessibility (left) [93]. However, Atrx–Daxx is also proposed to deposit H3.3 and to interact with Trim28, followed by H3.3 being marked with H3K9me3 by Eset (right) [95]

Back to article page