Tetsuji Kakutani

The paper shows that H2A variants guide heterochromatin formation in Arabidopsis, with H2A.W promoting and H2A.Z inhibiting it, while pericentromeric regions form heterochromatin autonomously.

The paper shows MBD8 binds LDL2 to facilitate H3K4me1 removal and transcriptional repression in H3K9me2-marked genes in Arabidopsis.

The paper investigates how natural genetic variation in Arabidopsis thaliana affects centromere-proximal crossover frequency and segregation distortion during meiosis.

This study shows H3K4me2 regulates H2A.Z and Polycomb repressive marks in Arabidopsis, influencing transcriptional repression and chromatin dynamics.

The paper shows that retrotransposons in Arabidopsis promote centromere function through epigenetically activated small RNAs, which are essential for chromosome segregation.

The paper shows H3K9me2 regulates silencing through incoherent feedforward loops involving H3K36me3 and H3K4me1.

This study reveals how DDM1 remodels H2A.W nucleosomes in Arabidopsis, enabling chromatin writers to access heterochromatin for DNA methylation.

The paper shows that RNAi targets noncoding regions of VANDAL TEs, while VANC proteins evolved to escape this silencing, suggesting a co-evolutionary arms race between TEs and host defense mechanisms.

The paper identifies three Arabidopsis methylases that direct H3K4me1 and shows their localization patterns are conserved in mice.

The paper shows that H2A.W and H3K9me work together with H1 and CH methylation to silence transposons in Arabidopsis.

Ultra-long-read sequencing resolves Arabidopsis centromeres, revealing their genetic and epigenetic structure and dynamics.

The paper investigates crosstalk among heterochromatin marks in Arabidopsis, showing that mCG guides mCH establishment and that global negative feedback regulates mCH targeting efficiency.

The paper identifies FLD as a histone demethylase that regulates bidirectional transcription in Arabidopsis by modulating H3K4me1 and DNA topology.