bioRxiv Science⌕ Search

Biology subjects

Masukagami, Y.

Publications and source records attributed to Masukagami, Y..

3 recordsLinked to original sources

Parallel Evolution of Bacteroidota as Long-Term Endosymbionts of Insects

Symbiotic relationships transform diverse aspects of both symbiont and host biology. The most visible changes include a massive reduction of the endosymbiont genome and the development of novel host organs, cells, and compartments specialized for harboring the symbionts. However, many insect symbiosis studies have previously focused either on Proteo-bacteria or only on a particular symbiosis stage, limiting our broad understanding of how and why symbiont diversity arises from specific microbial clades, how the symbiont genomes erode over evolutionary time, and what the consequences of symbiosis are for diverse host-symbiont pairs. Thanks to the repeated gains and losses of nutritional symbionts, scale insects provide an ideal evolutionary playground for tracking the parallel transitions of insect symbionts that originated as independent evolutionary replicates from the same bacterial phylum. Using extensive genome sampling across the scale insect phylogeny, we recapitulated the path of Bacteroidota transitioning from recently established host-associated bacteria to highly specialized insect endosymbionts with minimal gene sets. Their genomes exhibit strikingly parallel patterns of gene loss and pseudogenization across all gene categories, with some stochastic differences in essential genes for genetic processing and amino acid biosynthesis. In addition to the genetic transition, we show with imaging methods that the symbiotic cells and organs exhibit a trend from more dispersed bacteriocytes to highly compact (and likely more specialized) bacteriomes, which are closely localized to the hosts digestive system. Our results outline at both genomic and cellular levels a recurrent path by which insect symbioses independently arise, are temporarily maintained for up to several hundred million years, and then are replaced by new symbionts that repeat the process. The gradual nature of the process implies that the outcomes of symbiosis initially depend on how professional vs. naive the host and symbiont are. Over evolutionary time, compatible host-symbiont lineages emerge from these interactions and become preferred.

evolutionary biology↗

A Midichloriaceae endosymbiont of terrestrial arthropods found as an endosymbiont in a marine nematode

The obligate endosymbiont Candidatus Lariskella (Alphaproteobacteria, Candidatus Midichloriaceae) has been found across a wide diversity of terrestrial arthropods, including ticks, true bugs, beetles, fleas, wasps and moths. However, to date, Ca. Lariskella had never been detected in nematodes or marine animals. Here we report the first known occurrence of Ca. Lariskella infecting a population of marine nematodes (Enoplida, Thoracostomopsideae). This nematode-infecting Ca. Lariskella is closely related to insect-infecting Ca. Lariskella, despite the drastic shift in both host phylum and habitat. TEM and FISH microscopy showed Ca. Lariskella is localized within both somatic cells and developing oocytes, strongly suggesting that Ca. Lariskella is a vertically transmitted endosymbiont within the nematode population. We found that Ca. Lariskella was present within approximately 20% of the nematode population, but notably failed to detect any Ca. Lariskella within adult males, potentially hinting at reproductive manipulation. Overall, our findings show that Ca. Lariskella is not limited to arthropods or terrestrial hosts, indicating a larger host range than previously described. Its presence within marine nematodes demonstrates the ability of Ca. Lariskella to infect nematode hosts, as well as hosts from marine environments, suggesting terrestrial nematodes, marine arthropods, and perhaps even other marine invertebrates could be potential hosts of Ca. Lariskella.

microbiology↗

Plasma membrane damage limits replicative lifespan in yeast and human fibroblasts

Plasma membrane damage (PMD) occurs in all cell types due to environmental perturbation and cell-autonomous activities. However, cellular outcomes of PMD remain largely unknown except for recovery or death. Here, using budding yeast and normal human fibroblasts, we show that cellular senescence, irreversible cell cycle arrest contributing to organismal aging, is the long-term outcome of PMD. To identify the genes essential for PMD response, we developed a simple PMD-damaging assay using a detergent and performed a systematic yeast genome-wide screen. The screen identified 48 genes. The top hits in the screen are the endosomal sorting complexes required for transport (ESCRT) genes, encoding the well-described plasma membrane repair proteins in eukaryotes. Unexpectedly, the replicative lifespan regulator genes are enriched in our 48 hits. This finding suggests a close genetic association between the PMD response and the replicative lifespan regulations. Indeed, we show that PMD limits the replicative lifespan in budding yeast; the ESCRT activator AAA-ATPase VPS4-overexpression extends it. These results suggest that PMD limits replicative lifespan in budding yeast. Moreover, in normal human fibroblasts, we find that PMD induces premature senescence via the Ca2+-p53 axis but not the major senescence pathway, ATM/ATR pathway. Consistent with the results in yeast, transient overexpression of ESCRT-III, CHMP4B, suppressed the PMD-dependent senescence in normal human fibroblasts. Our study proposes that PMD limits cellular lifespan in two different eukaryotic cell types and highlights an underappreciated but ubiquitous senescent cell subtype, namely PMD-dependent senescent cells.

cell biology↗