Biomedical subjects

Shin Takagi

Publications and source records attributed to Shin Takagi.

4 recordsLinked to original sources

PubMed2007

Improved method for visualizing cells revealed dynamic morphological changes of ventral neuroblasts during ventral cleft closure of Caenorhabditis elegans.

The formation of intricate and functional biological structures depends on the dynamic changes of cellular morphology. Confocal laser scanning microscopy (CLSM) is a widely used method to reveal the three-dimensional (3-D) structure of cells during the development of Caenorhabditis elegans (C. elegans) and other model organisms. Improving the efficiency and image quality of CLSM would benefit studies using this method. We found that CED-10::GFP::CED-10, a green fluorescent protein (GFP) marker, is intensely expressed beneath the cell surface, facilitating visualization of cellular morphology in C. elegans embryos. By combining the unique properties of this marker, and with the help of direct 3-D rendering of images obtained by CLSM, we developed a simple but powerful method for investigating cellular morphology in developing embryos. Using this method we, for the first time, document the dynamic changes in the morphology of ventral neuroblasts in vivo during ventral cleft closure.

Animals↗

PubMed2005

C. elegans PlexinA PLX-1 mediates a cell contact-dependent stop signal in vulval precursor cells.

PLX-1 is a PlexinA transmembrane protein in Caenorhabditis elegans, and the transmembrane-type semaphorin, SMP-1, is a ligand for PLX-1. The SMP-1/PLX-1 system has been shown to be necessary for proper epidermal morphogenesis in the male tail and seam cells. Here, we show that the SMP-1/PLX-1 system also regulates vulval morphogenesis. In plx-1 and smp-1 mutants, hermaphrodites sometimes exhibit a protruding vulva or multiple vulva-like protrusions. Throughout the vulval development of plx-1 and smp-1 mutants, the arrangement of vulval cells is often disrupted. In the initial step of vulval morphogenesis, vulval precursor cells (VPCs) are generated normally but are subsequently arranged abnormally in mutants. Continuous observation revealed that plx-1 VPC fails to terminate longitudinal extension after making contact with neighbor VPCs. The arrangement defects of VPCs in plx-1 and smp-1 mutants are rescued by expressing the respective cDNA in VPCs. plx-1::egfp and smp-1::egfp transgenes are both expressed in all vulval cells, including VPCs, throughout vulval development. We propose that the SMP-1/PLX-1 system is responsible for a cell contact-mediated stop signal for VPC extension. Analyses using cell fate-specific markers showed that the arrangement defects of VPCs also affect cell fate specification and cell lineages, but in a relatively small fraction of plx-1 mutants.

Animals↗

PubMed2004

mau-2 acts cell-autonomously to guide axonal migrations in Caenorhabditis elegans.

The gene mau-2 has been found to be required for the guidance of cellular and axonal migrations along both the anteroposterior and the dorsoventral body axes during the development of the nematode C. elegans. We show that mau-2 encodes a novel, previously uncharacterized protein that is highly conserved among animals. Maternal mau-2 gene expression is sufficient for normal development until the fourth larval stage, and a MAU-2::GFP fusion protein localizes to the cytoplasm of neurones. mau-2 is ubiquitously expressed in embryos by late gastrulation and becomes predominantly expressed in the nervous system as morphogenesis progresses. Expression of mau-2 within individual neurones rescues the guidance defects of mau-2 mutants, indicating that mau-2 functions cell-autonomously. Altering the activity of both the dorsal repellent slt-1 and mau-2 leads to the abnormal dorsal projection of the AVM axon, a phenotype that is novel and specific to the interaction of these two genes, indicating that mau-2 participates in the guidance of AVM by a slt-1-independent mechanism. Taken together, mau-2 defines a novel guidance factor that might be involved in the intracellular processing of guidance cues encountered by migrating cells and axons during development.

Alleles↗

PubMed2002

Caenorhabditis elegans PlexinA, PLX-1, interacts with transmembrane semaphorins and regulates epidermal morphogenesis.

The plexin family transmembrane proteins are putative receptors for semaphorins, which are implicated in the morphogenesis of animal embryos, including axonal guidance. We have generated and characterized putative null mutants of the C. elegans plexinA gene, plx-1. plx-1 mutants exhibited morphological defects: displacement of ray 1 and discontinuous alae. The epidermal precursors for the affected organs were aberrantly arranged in the mutants, and a plx-1::gfp transgene was expressed in these epidermal precursor cells as they underwent dynamic morphological changes. Suppression of C. elegans transmembrane semaphorins, Ce-Sema-1a and Ce-Sema-1b, by RNA interference caused a displacement of ray 1 similar to that of plx-1 mutants, whereas mutants for the Ce-Sema-2a/mab-20 gene, which encodes a secreted-type semaphorin, exhibited phenotypes distinct from those of plx-1 mutants. A heterologous expression system showed that Ce-Sema-1a, but not Ce-Sema-2a, physically bound to PLX-1. Our results indicate that PLX-1 functions as a receptor for transmembrane-type semaphorins, and, though Ce-Sema-2a and PLX-1 both play roles in the regulation of cellular morphology during epidermal morphogenesis, they function rather independently.

Amino Acid Sequence↗