Biology subjects

Kayama, M.

Publications and source records attributed to Kayama, M..

3 recordsLinked to original sources

bioRxiv2025

Somatic gene repression ensures physical segregation of germline and soma in Drosophila embryos

In many animals, primordial germ cells are transiently segregated outside the somatic-cell cluster that forms the embryos body during early embryogenesis. This physical segregation of germline from the soma has been long believed to be crucial for germline development, but the mechanisms controlling this segregation and its developmental significance remain unclear. Here, in Drosophila, we show that somatic gene silencing in the germline is essential for maintaining this segregation. We showed that primordial germ cells (pole cells) lacking the Nanos- and Polar granule component (Pgc)-dependent dual repression mechanism caused misexpression of widespread somatic genes. They formed abnormal cellular protrusions, invaded adjacent somatic epithelium, and intermingled with somatic cells. These mislocalized pole cells ultimately underwent cell death, whereas properly segregated cells survived. Notably, the knockdown of miranda (mira), one of the somatic genes expressed ectopically in the pole cells lacking this repression mechanism, rescued these phenotypes. Our findings provide the first evidence that somatic gene silencing in germline is essential for preserving the physical segregation between germline and soma, highlighting its role in ensuring germline viability during early development.

developmental biology↗

bioRxiv2021

Genome evolution of a non-parasitic secondary heterotroph, the diatom Nitzschia putrida

Secondary loss of photosynthesis is observed across almost all plastid-bearing branches of the eukaryotic tree of life. However, genome-based insights into the transition from a phototroph into a secondary heterotroph have so far only been revealed for parasitic species. Free-living organisms can yield unique insights into the evolutionary consequence of the loss of photosynthesis, as the parasitic lifestyle requires specific adaptations to host environments. Here we report on the diploid genome of the free-living diatom Nitzschia putrida (35 Mbp), a non-photosynthetic osmotroph whose photosynthetic relatives contribute ca. 40% of net oceanic primary production. Comparative analyses with photosynthetic diatoms revealed that a combination of genes loss, the horizontal acquisition of genes involved in organic carbon degradation, a unique secretome and the rapid divergence of conserved gene families involved in cell wall and extracellular metabolism appear to have facilitated the lifestyle of a non-parasitic, free-living secondary heterotroph.

genomics↗

bioRxiv2018

Combined inhibition of apoptosis and necrosis promotes transient neuroprotection of retinal ganglion cells and partial axon regeneration after optic nerve damage

Retinal ganglion cell (RGC) death is the hallmark of glaucoma. Axonal injury is thought to precede RGC loss in glaucoma, and thus studies using an optic nerve (ON) crush model have been widely used to investigate mechanisms of cell death that are common to both conditions. Prior work has focused on the involvement of caspases in RGC death, but little is known about the contribution of other forms of cell death such as necrosis. In this study we show that receptor interacting protein (RIP) kinase-mediated necrosis normally plays a role in RGC death and acts in concert with caspase-dependent apoptosis. The expression of RIP3, a key activator of RIP1 kinase, as well as caspase activity, increased following ON injury. Caspase inhibition alone failed to provide substantial protection to injured RGCs and unexpectedly exacerbated necrosis. In contrast, pharmacologic or genetic inhibition of RIP kinases in combination with caspase blockade delayed both apoptotic and necrotic RGC death, although RGCs still continued to die. Furthermore, inhibition of RIP1 kinase promoted a moderate level of axon regeneration that was only minimal affected by caspase inhibition. In conclusion, multiple approaches are required for effective RGC death prevention and axonal regeneration. Further studies are needed to elucidate more effective long term strategies that can lead to sustained neuroprotection and regeneration.

neuroscience↗