Biology subjects

Le, Q. T.

Publications and source records attributed to Le, Q. T..

4 recordsLinked to original sources

bioRxiv2026

A chromosome-scale reference genome and single-nucleus root atlas reveal the cellular and molecular basis of coastal adaptation in sand bean (Strophostyles helvola)

Plants adapted to saline coastal habitats provide valuable systems for understanding how natural selection reshapes stress-response programs, yet the cellular and molecular basis of this adaptation remains poorly resolved. Here, we generated a chromosome-scale reference genome and a single-nucleus transcriptomic atlas of roots from sand bean (Strophostyles helvola), a wild legume represented by salt-tolerant Beach and salt-sensitive Inland ecotypes. The atlas comprised 87,901 nuclei assigned to 25 transcriptional clusters representing 16 major root cell types. Salt exposure elicited cell-type-specific transcriptional responses that differed between Beach and Inland roots. Beach roots preferentially maintained respiration-, energy metabolism-, and protein-homeostasis-associated functions, whereas Inland roots showed stronger induction of canonical abiotic-stress, ABA, water-deficit, hypoxia, and oxidative-stress programs. Integrating baseline ecotype differences with salt-responsive expression revealed that many genes induced by salt in Inland roots were already expressed at higher levels in untreated Beach roots. This baseline-enriched configuration comprised a broadly distributed regulatory backbone, including ERF-family transcription factors and RING-type E3 ubiquitin ligases, together with cell-type-associated modules involving ion and water transport at the root-soil interface, redox and dehydration protection in outer-root tissues, endodermal barrier-associated genes, and vascular regulatory candidates. These findings support a model in which Beach salt tolerance is associated not with entirely distinct stress-response pathways, but with the pre-existing and spatially organized deployment of conserved protective programs that remain responsive to salt exposure. Our study establishes genomic and cellular resources for sand beans and provides a framework for investigating how natural variation in the regulation and cellular organization of conserved pathways contributes to environmental stress tolerance.

plant biology↗

bioRxiv2026

Apoptotic bodies from patients with Sjogren's disease drive atypical memory B cell and macrophage activation and autoantibody production

The impaired clearance of apoptotic cells has long been associated with systemic autoimmune diseases like Sjogrens disease (SjD), which is characterised by autoantibodies targeting antigens on apoptotic cells. However, most studies analysing human samples have used patient-derived phagocytes and in vitro generated apoptotic cells, which do not reflect the heterogeneity of patient-derived apoptotic bodies (ApoBDs). Here, we molecularly and functionally compare ApoBDs derived from patients with SjD and healthy donors. ApoBDs were increased in the circulation in SjD and induced atypical memory B cell expansion, which was attenuated by blocking B cell receptor (BCR) and Toll-like receptors (TLR) 7-9 signalling. Co-cultures of ApoBDs and B cells drove autoantibody production. Macrophages engulfing SjD ApoBDs had a distinct inflammatory profile compared to macrophages engulfing healthy control ApoBDs. These findings define patient-derived ApoBDs as immunostimulatory substrates capable of driving innate and adaptive immune responses consistent with the pathogenic features observed in SjD, hence opening a new avenue of diagnostic and therapeutic development.

immunology↗

bioRxiv2021

Aldehyde dehydrogenase 3A1 deficiency leads to mitochondrial dysfunction and impacts salivary gland stem cell self-renewal, differentiation and survival

Adult salivary stem/progenitor cells (SSPC) have an intrinsic property to self-renew in order to maintain tissue architecture and homeostasis. Adult salivary glands have been documented to harbor SSPC, which have been shown to play a vital role in the regeneration of the glandular structures post radiation damage. We have previously demonstrated that activation of aldehyde dehydrogenase 3A1 (ALDH3A1) after radiation reduced aldehyde accumulation in SSPC, leading to less apoptosis and improved salivary function. We subsequently found that sustained pharmacological ALDH3A1 activation is critical to enhance regeneration of murine submandibular gland after radiation damage. Further investigation shows that ALDH3A1 function is crucial for SSPC self-renewal and differentiation even in the absence of radiation stress. Salivary glands from Aldh3a1-null mice have fewer acinar structures than wildtype mice. ALDH3A1 deletion or pharmacological inhibition in SSPC leads to a decrease in mitochondrial DNA copy number, lower expression of mitochondrial specific genes and proteins, structural abnormalities, lower membrane potential, and reduced cellular respiration. Loss or inhibition of ALDH3A1 also elevates ROS levels and accumulation of ALDH3A1 substrate 4-hydroxynonenal (4-HNE, a lipid peroxidation product), leading to decreased survival of murine SSPC that can be rescued by treatment with 4-HNE specific carbonyl scavengers. Our data indicate that ALDH3A1 activity protects mitochondrial function and is important for the development and regeneration activity of SSPC. This knowledge will help to guide our translational strategy of applying ALDH3A1 activators in the clinic to prevent radiation-related hyposalivation in head and neck cancer patients.

cell biology↗

bioRxiv2021

The within-host evolutionary dynamics of seasonal and pandemic human influenza A viruses in young children

The evolution of influenza viruses is fundamentally shaped by within-host processes. However, the within-host evolutionary dynamics of influenza viruses remain incompletely understood, in part because most studies have focused on within-host virus diversity of infections in otherwise healthy adults based on single timepoint data. Here, we analysed the within-host evolution of 82 longitudinally-sampled individuals, mostly young children, infected with A/H3N2 or A/H1N1pdm09 viruses between 2007 and 2009. For A/H1N1pdm09 infections during the 2009 pandemic, nonsynonymous changes were common early in infection but decreased or remained constant throughout infection. For A/H3N2 viruses, early infection was dominated by purifying selection. However, as infections progressed, nonsynonymous variants increased in frequencies even though within-host virus titres decreased, leading to the maintenance of virus diversity via mutation-selection balance. Our findings suggest that this maintenance of genetic diversity in these children combined with their longer duration of infection may provide important opportunities for within-host virus evolution.

microbiology↗