Biology subjects

XU, X.

Publications and source records attributed to XU, X..

3 recordsLinked to original sources

bioRxiv2026

Plaque microbial community restructuring in rampant dental caries after exclusion of a confirmed Streptococcus mutans ASV: an analysis of public 16S rRNA sequencing data

Background: Dental caries is increasingly understood as an ecological biofilm disorder rather than the consequence of a single organism. Although Streptococcus mutans is strongly implicated in cariogenesis, it remains unclear whether caries-associated plaque-community differences persist beyond this organism. Methods: We reanalysed publicly available supragingival-plaque 16S rRNA sequencing data from 88 preschool children with rampant caries (n=44) or who were caries-free (n=44; BioProject PRJNA1141721). Single-end DADA2 processing yielded 25,669 amplicon sequence variants (ASVs), including one ASV confirmed as S. mutans by an eHOMD reference-window procedure. The pre-specified primary analysis compared Bray-Curtis community composition after exclusion of this ASV. Results: Non-S. mutans community composition differed between groups (PERMANOVA pseudo-R2=0.0462, pseudo-F=4.16, P<0.001), without evidence of unequal multivariate dispersion (P=0.796); rarefaction produced a nearly identical result. Shannon diversity did not differ (P=0.486). The confirmed S. mutans ASV was detected in 8/44 rampant-caries and 42/44 caries-free samples and was lower in abundance in rampant caries. Among 758 prevalence-filtered non-S. mutans ASVs, 239 showed conventional FDR-significant differential abundance, with more showing lower than higher bias-corrected abundance in rampant caries (176 versus 63); 239 additional ASVs were classified as structural zeros. Individual ASV findings were sensitive to prevalence filtering. Adjustment for S. mutans abundance attenuated the global caries-group association (marginal pseudo-R2=0.0149, P=0.085) in the presence of strong collinearity. Conclusions: Rampant caries was associated with modest but reproducible plaque-community restructuring after exclusion of a confirmed S. mutans ASV, without a corresponding Shannon-diversity difference. These findings support a community-level ecological interpretation but do not establish statistical independence from S. mutans or a causal role for individual taxa.

microbiology↗

bioRxiv2025

Squash ensures Spindle-E-dependent heterotypic ping-pong amplification of piRNAs in the Drosophila ovary

The PIWI-interacting RNA (piRNA) pathway plays a crucial role in repressing mobile transposable elements (TEs) and protecting the integrity of the heritable genome in animal gonads. In the Drosophila ovary, piRNAs are produced in a membrane-less organelle called nuage, in which many piRNA factors are localized. Among them, Squash (Squ) has also been identified as a key component in piRNA-directed TE silencing. However, its molecular function remains largely unknown. Here, we demonstrate that loss of Squ leads to defective piRNA biogenesis, which is associated with the abnormal accumulation of precursor transcripts and the specific destabilization of Ago3, a member of the PIWI-family proteins. Reducing Ago3 results in enhanced homotypic piRNA amplification mediated by Aub itself, rather than the heterotypic ping-pong amplification between Aub and Ago3. Additionally, we demonstrate that Squ is a functional cofactor of the RNA helicase, Spindle-E (Spn-E), which plays a vital role in piRNA biogenesis. Point mutations that abrogate the interaction between Squ and Spn-E result in TE de-repression and defective precursor processing, suggesting that Squ works with Spn-E to ensure the proper piRNA biogenesis. These results identify Squ as a critical factor for Spn-E-dependent heterotypic ping-pong amplification of piRNAs in the Drosophila ovary.

cell biology↗

bioRxiv2024

Nucleotidyltransferase toxin MenT targets and extends the aminoacyl acceptor ends of serine tRNAs in vivo to control Mycobacterium tuberculosis growth

Toxins of toxin-antitoxin systems use diverse mechanisms to control bacterial growth and represent attractive therapeutic targets to fight pathogens. In this study, we characterized the translation inhibitor toxin MenT3 of Mycobacterium tuberculosis, the bacterium responsible for human tuberculosis in humans. We show that MenT3 is a robust cytidine specific tRNA nucleotidyltransferase in vitro, capable of modifying the aminoacyl acceptor ends of most tRNA but with a marked preference for tRNASer, to which long stretches of cytidines were added. Furthermore, transcriptomic-wide analysis of MenT3 targets in M. tuberculosis identified tRNASer as the sole target of MenT3 in vivo and revealed significant detoxification attempts by ribonuclease PH in response to MenT3 overexpression. Finally, under physiological conditions, only in the presence the native menAT3 operon, we found the unexpected presence of an active pool of endogenous MenT3 targeting tRNASer in M. tuberculosis, likely reflecting the importance of MenT3 during infection.

microbiology↗