Shigeki Iwase

This study shows RAI1 deficiency accelerates human neurodevelopmental gene expression and disrupts lineage programs in neural progenitors.

This study identifies distinct roles of H3K4 methyltransferases in synaptic scaling, showing that different KMT2 subfamilies are required for upscaling or downscaling.

The paper identifies neuron-specific microexon splicing in chromatin regulators, showing that PHF21A loses DNA-binding function in neurons while retaining H3K4me0 recognition, contributing to brain development.

The paper investigates how KDM5C regulates germline gene repression in somatic cells, revealing sex-biased mechanisms and distinct regulatory classes of germline genes.

The paper shows that the X-Y gene pair Kdm5c-Kdm5d regulates sex-biased gene expression in mouse ESCs, with loss of either gene neutralizing sex bias.

The paper shows that PHF21A microexon expression precedes LSD1 microexon expression during neurodevelopment, leading to stepwise deactivation of the LSD1-PHF21A complex and unique gene-regulatory roles in neurons.

The paper demonstrates successful CRISPR genome editing in the Nile grass rat, a diurnal rodent, establishing methods for reproductive and genetic manipulation.

The paper identifies alcohol-specific transcriptional changes during memory reconsolidation using mouse models and RNA-sequencing.

This study shows LSD1/KDM1A suppresses primed enhancers in mESC by maintaining H3K4me1 levels and preventing aberrant enhancer activity.

The paper profiles nascent RNA in neuronal cultures to show activity-dependent transcriptional changes and links RAI1 to synaptic scaling mechanisms.

This study shows that shRNAs cause microRNA dysregulation and global transcriptomic changes in neurons, independent of their target.

This study shows that KMT2A and KDM5C, which have opposing enzymatic activities, work together to regulate neuronal structure, behavior, and H3K4 methylation, with their combined loss reversing some phenotypes.

This study shows that SMCX/KDM5C, a histone demethylase, is required for X-inactivation in female mammals by inducing Xist RNA and silencing X-linked genes.