Drosophila Alpha-ketoglutarate-dependent dioxygenase AlkB is involved in repair from neuronal disorders induced by ultraviolet damage.

AlkB family proteins are enzymes that repair alkylated DNA and RNA by oxidative demethylation. Nine homologs have been identified and characterized in mammals. ALKBH1 is conserved among metazoans including Drosophila.

The dawn of pirna research in various neuronal disorders.

Small non-coding PIWI-interacting RNAs (piRNAs) silence the expression of transposable elementsof eukaryotic genomes in germline cells. Additionally, piRNAs regulate chromatin modifications, such as trimethylation of histone H3 lysine 9　(H3K9me3) or DNA methylation. In the past decade, the roles of piRNAs have been characterized in somatic cells, including post-mitotic neurons.

Novel roles of Drosophila FUS and Aub responsible for piRNA biogenesis in neuronal disorders.

piRNAs, small non-coding RNAs, were considered to be restricted to germline cells. Although they have recently been detected in somatic cells including neurons, it remains unclear how piRNA biogenesis is involved in neuronal diseases. We herein examined the possible roles of Aubergine (Aub), a Piwi-family protein (PIWI) responsible for piRNA biogenesis, in the neuronal disorders, using the Cabeza (Caz) knockdown Drosophila.

Association of zygotic piRNAs derived from paternal elements with hybrid dysgenesis in .

Background: -element transposition in the genome causes P-M hybrid dysgenesis in . Maternally deposited piRNAs suppress -element transposition in the progeny, linking them to P-M phenotypes; however, the role of zygotic piRNAs derived from paternal elements is poorly understood.

Results: To elucidate the molecular basis of -element suppression by zygotic factors, we investigated the genomic constitution and -element piRNA production derived from fathers.

Diversity of element piRNA production among M' and Q strains and its association with P-M hybrid dysgenesis in .

Background: Transposition of elements in the genome causes P-M hybrid dysgenesis in . For the P strain, the P-M phenotypes are associated with the ability to express a class of small RNAs, called piwi-interacting small RNAs (piRNAs), that suppress the elements in female gonads. However, little is known about the extent to which piRNAs are involved in the P-M hybrid dysgenesis in M' and Q strains, which show different abilities to regulate the elements from P strains.

Identification and functional characterization of KCNQ1 mutations around the exon 7-intron 7 junction affecting the splicing process.

Background: KCNQ1 gene encodes the delayed rectifier K(+) channel in cardiac muscle, and its mutations cause long QT syndrome type 1 (LQT1). Especially exercise-related cardiac events predominate in LQT1. We previously reported that a KCNQ1 splicing mutation displays LQT1 phenotypes.