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Nishiwaki, K.

Publications and source records attributed to Nishiwaki, K..

2 recordsLinked to original sources

Repulsive Guidance Molecule Acts in Axon Branching in Caenorhabditis elegans

Repulsive guidance molecules (RGMs) are evolutionarily conserved proteins implicated in repulsive axon guidance. Here we report the function of the Caenorhabditis elegans ortholog DRAG-1 in axon branching. The axons of hermaphrodite-specific neurons (HSNs) branch at the region abutting the vulval muscles and innervate these muscles to control egg laying. The drag-1 mutants exhibited defects in HSN axon branching in addition to a small body size and egg laying-defective phenotype. DRAG-1 expression in the hypodermal cells was required for the branching of these axons. The C-terminal glycosylphosphatidylinositol anchor of DRAG-1 was important for its function. Genetic analyses suggested that the membrane receptor UNC-40, but neither SMA-1/{beta}H-spectrin nor SMA-5/MAP kinase 7, acts in the same pathway with DRAG-1 in HSN branching. We propose that DRAG-1 expressed in the hypodermis signals via the UNC-40 receptor expressed in HSNs to elicit branching activity of HSN axons.

developmental biology

Maintenance of Cell Fates by Regulation of the Histone Variant H3.3 in Caenorhabditis elegans

HighlightsTLK-1 maintains cell fates by repression of selector genes\n\nTLK-1 and downstream H3 chaperone CAF1 inhibit H3.3 deposition\n\nLoss of sin-3 suppresses the defect in cell-fate maintenance of tlk-1 mutants\n\nAcH4-binding protein BET-1 is necessary for sin-3 suppression\n\nSummaryCell-fate maintenance is important to preserve the variety of cell types that are essential for the formation and function of tissues. We previously showed that the acetylated histone H4-binding protein BET-1 maintains cell fate by recruiting the histone variant H2A.z. Here, we report that Caenorhabditis elegans tousled-like kinase TLK-1 and the histone H3 chaperone CAF1 maintain cell fate by preventing the incorporation of histone variant H3.3 into nucleosomes, thereby repressing ectopic expression of transcription factors that induce cell-fate specification. Genetic analyses suggested that TLK-1 and BET-1 act in parallel pathways. In tlk-1 mutants, the loss of SIN-3, which promotes histone acetylation, suppressed a defect in cell-fate maintenance in a manner dependent on MYST family histone acetyltransferase MYS-2 and BET-1. sin-3 mutation also suppressed abnormal H3.3 incorporation. Thus, we propose that the regulation and interaction of histone variants play crucial roles in cell-fate maintenance through the regulation of selector genes.

developmental biology