Limits...
Distinct mechanisms determine transposon inheritance and methylation via small interfering RNA and histone modification.

Lippman Z, May B, Yordan C, Singer T, Martienssen R - PLoS Biol. (2003)

Bottom Line: More recently, transposon silencing has been associated with DNA methylation, histone H3 lysine-9 methylation (H3mK9), and RNA interference (RNAi).According to their pattern of transposon regulation, the mutants can be divided into two groups, which suggests that there are distinct, but interacting, complexes or pathways involved in transposon silencing.Furthermore, different transposons tend to be susceptible to different forms of epigenetic regulation.

View Article: PubMed Central - PubMed

Affiliation: Cold Spring Harbor Laboratory, Cold Spring Harbor, New York, USA.

ABSTRACT
Heritable, but reversible, changes in transposable element activity were first observed in maize by Barbara McClintock in the 1950s. More recently, transposon silencing has been associated with DNA methylation, histone H3 lysine-9 methylation (H3mK9), and RNA interference (RNAi). Using a genetic approach, we have investigated the role of these modifications in the epigenetic regulation and inheritance of six Arabidopsis transposons. Silencing of most of the transposons is relieved in DNA methyltransferase (met1), chromatin remodeling ATPase (ddm1), and histone modification (sil1) mutants. In contrast, only a small subset of the transposons require the H3mK9 methyltransferase KRYPTONITE, the RNAi gene ARGONAUTE1, and the CXG methyltransferase CHROMOMETHYLASE3. In crosses to wild-type plants, epigenetic inheritance of active transposons varied from mutant to mutant, indicating these genes differ in their ability to silence transposons. According to their pattern of transposon regulation, the mutants can be divided into two groups, which suggests that there are distinct, but interacting, complexes or pathways involved in transposon silencing. Furthermore, different transposons tend to be susceptible to different forms of epigenetic regulation.

Show MeSH

Related in: MedlinePlus

Model of Transposon Silencing Complexes(A) DDM1, MET1, and SIL1 are all required for transposon silencing and may interact. MET1 and DDM1 are also required for siRNA accumulation (shown in red). AGO and KYP have similar effects on transposon activation and may also interact. They impact DNA methylation via CMT3 (Cao and Jacobsen 2002; Jackson et al. 2002).(B) siRNA, histone H3 methylation, and DNA methylation interact to silence transposons. Silencing is maintained by the MET1/DDM1/SIL1 complex. A possible network is shown.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC300680&req=5

pbio.0000067-g005: Model of Transposon Silencing Complexes(A) DDM1, MET1, and SIL1 are all required for transposon silencing and may interact. MET1 and DDM1 are also required for siRNA accumulation (shown in red). AGO and KYP have similar effects on transposon activation and may also interact. They impact DNA methylation via CMT3 (Cao and Jacobsen 2002; Jackson et al. 2002).(B) siRNA, histone H3 methylation, and DNA methylation interact to silence transposons. Silencing is maintained by the MET1/DDM1/SIL1 complex. A possible network is shown.

Mentions: We have taken a genetic approach to dissecting transposon regulation. By examining representative transposons of each class in each mutant, we demonstrate first that transposons differ in their regulation. Next, we show that the mutants can be grouped according to their pattern of transposon regulation, revealing two distinct mechanisms of transposon silencing (Figure 5A). kyp resembles ago1-9 in that it is only required to silence a subset of transposons, even though kyp results in widespread loss of H3mK9. met1 and ddm1 resemble each other and sil1 more closely than cmt3, ago1, and kyp. In sil1, H3mK9 is lost, but unlike in kyp, most of the elements are derepressed. SIL1 encodes the HDAC HDA6 (H. Vaucheret, O. Mittelsten-Scheid, and I. Furner, personal communication), which has been implicated in posttranscriptional gene silencing (Murfett et al. 2001) as well as in RNA-directed DNA methylation (Aufsatz et al. 2002).


Distinct mechanisms determine transposon inheritance and methylation via small interfering RNA and histone modification.

Lippman Z, May B, Yordan C, Singer T, Martienssen R - PLoS Biol. (2003)

Model of Transposon Silencing Complexes(A) DDM1, MET1, and SIL1 are all required for transposon silencing and may interact. MET1 and DDM1 are also required for siRNA accumulation (shown in red). AGO and KYP have similar effects on transposon activation and may also interact. They impact DNA methylation via CMT3 (Cao and Jacobsen 2002; Jackson et al. 2002).(B) siRNA, histone H3 methylation, and DNA methylation interact to silence transposons. Silencing is maintained by the MET1/DDM1/SIL1 complex. A possible network is shown.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC300680&req=5

pbio.0000067-g005: Model of Transposon Silencing Complexes(A) DDM1, MET1, and SIL1 are all required for transposon silencing and may interact. MET1 and DDM1 are also required for siRNA accumulation (shown in red). AGO and KYP have similar effects on transposon activation and may also interact. They impact DNA methylation via CMT3 (Cao and Jacobsen 2002; Jackson et al. 2002).(B) siRNA, histone H3 methylation, and DNA methylation interact to silence transposons. Silencing is maintained by the MET1/DDM1/SIL1 complex. A possible network is shown.
Mentions: We have taken a genetic approach to dissecting transposon regulation. By examining representative transposons of each class in each mutant, we demonstrate first that transposons differ in their regulation. Next, we show that the mutants can be grouped according to their pattern of transposon regulation, revealing two distinct mechanisms of transposon silencing (Figure 5A). kyp resembles ago1-9 in that it is only required to silence a subset of transposons, even though kyp results in widespread loss of H3mK9. met1 and ddm1 resemble each other and sil1 more closely than cmt3, ago1, and kyp. In sil1, H3mK9 is lost, but unlike in kyp, most of the elements are derepressed. SIL1 encodes the HDAC HDA6 (H. Vaucheret, O. Mittelsten-Scheid, and I. Furner, personal communication), which has been implicated in posttranscriptional gene silencing (Murfett et al. 2001) as well as in RNA-directed DNA methylation (Aufsatz et al. 2002).

Bottom Line: More recently, transposon silencing has been associated with DNA methylation, histone H3 lysine-9 methylation (H3mK9), and RNA interference (RNAi).According to their pattern of transposon regulation, the mutants can be divided into two groups, which suggests that there are distinct, but interacting, complexes or pathways involved in transposon silencing.Furthermore, different transposons tend to be susceptible to different forms of epigenetic regulation.

View Article: PubMed Central - PubMed

Affiliation: Cold Spring Harbor Laboratory, Cold Spring Harbor, New York, USA.

ABSTRACT
Heritable, but reversible, changes in transposable element activity were first observed in maize by Barbara McClintock in the 1950s. More recently, transposon silencing has been associated with DNA methylation, histone H3 lysine-9 methylation (H3mK9), and RNA interference (RNAi). Using a genetic approach, we have investigated the role of these modifications in the epigenetic regulation and inheritance of six Arabidopsis transposons. Silencing of most of the transposons is relieved in DNA methyltransferase (met1), chromatin remodeling ATPase (ddm1), and histone modification (sil1) mutants. In contrast, only a small subset of the transposons require the H3mK9 methyltransferase KRYPTONITE, the RNAi gene ARGONAUTE1, and the CXG methyltransferase CHROMOMETHYLASE3. In crosses to wild-type plants, epigenetic inheritance of active transposons varied from mutant to mutant, indicating these genes differ in their ability to silence transposons. According to their pattern of transposon regulation, the mutants can be divided into two groups, which suggests that there are distinct, but interacting, complexes or pathways involved in transposon silencing. Furthermore, different transposons tend to be susceptible to different forms of epigenetic regulation.

Show MeSH
Related in: MedlinePlus