Biology subjects

Wen, F.

Publications and source records attributed to Wen, F..

8 recordsLinked to original sources

bioRxiv2026

High frequency of apomixis in subterranean islands challenges macro-climatic models of geographical parthenogenesis

The Geographical Parthenogenesis (GP) hypothesis traditionally links apomixis to high-latitude and alpine regions, driven by a combination of thermal stress, UV radiation, and pollination barriers. At the core of the GP hypothesis is Bakers Law, which asserts the evolutionary advantage of autonomous reproduction during the colonization of isolated habitats, frequently linking this advantage to macro-climatic stress. By investigating reproductive modes in subtropical subterranean karst caves, we test the core assumption that macro-climatic stress is the primary driver of apomixis. Our results suggest that barriers to pollination drive a high frequency of apomixis independently of thermal stress or UV radiation. Furthermore, we find a complete phylogenetic turnover between high-elevation, open, apomict-rich habitats and mid-elevation cave environments. Taxonomic composition in these caves is dictated by pre-adaptations to deep shade combined with a lineage-specific predisposition for autonomous reproduction. We propose that the GP hypothesis may be overly influenced by habitat sampling bias. Broader, unbiased sampling could yield a more nuanced and predictive framework to explain variations in apomixis frequency, ultimately providing deeper insights into the role of asexual reproduction in evolution

evolutionary biology↗

bioRxiv2026

Viral rewiring of DDR signaling activates a pro-survival network that drives chemotherapy resistance

Radiation and chemotherapy rely on an intact DNA damage response (DDR) to halt cell-cycle progression and eliminate damaged cells, yet many tumors evade these outcomes and develop resistance. Adenoviruses remodel host signaling networks in ways that mirror tumor evolution, providing a powerful system to dissect how DDR pathways are subverted. Here, we identify two scenarios in which the central DDR kinases ATM and ATR are reprogrammed from enforcing CHK1/CHK2-dependent checkpoint arrest to activating a NEMO-NF-{kappa}B survival pathway. This rewiring induces transcriptional programs associated with stress tolerance, anti-apoptotic signaling, and chemoresistance, and promotes the accumulation of cells with abnormal DNA content. These findings reveal a previously unrecognized mode of DDR plasticity that generates a pro-survival state reminiscent of early tumor evolution and suggest how ATM- and ATR-dependent pathways can be co-opted to promote therapeutic resistance.

molecular biology↗

bioRxiv2026

RIPK3 suppresses photoreceptor degeneration in a Stargardt disease mouse model

Autosomal recessive Stargardt disease type 1 (STGD1) is the most prevalent inherited juvenile macular degeneration, ultimately leading to irreversible blindness through photoreceptor cell loss, yet the underlying cell death mechanisms remain poorly defined. Receptor-interacting protein kinase 3 (RIPK3) is a well-established mediator of necroptosis and, under certain circumstances, apoptosis downstream of TNF family ligands, and it was found to be progressively upregulated in the retina of a STGD1 abca4-/-rdh8-/- (DKO) mouse model coinciding with the onset and progression of photoreceptor degeneration. Despite elevated RIPK3 expression, necroptosis was not detectable in this model, as evidenced by the absence of phosphorylated MLKL and unaltered photoreceptor degeneration in abca4-/- rdh8-/-mlkl-/- mice. Intriguingly, genetic ablation of Ripk3 exacerbated photoreceptor loss in DKO mice in both chronic (age-dependent) and acute (light-induced) retinal degeneration paradigms. This detrimental effect was partially ameliorated by pan-caspase inhibition in the acute degeneration model, indicating caspase-dependent apoptosis as the primary executioner. Mechanistically, we demonstrated that RIPK3 suppressed extrinsic apoptosis by attenuating caspase-8 activation downstream of TNF family ligands. Collectively, our findings reveal a non-canonical, protective role of RIPK3 in photoreceptors, as a brake on apoptotic signaling rather than a necroptotic executor, in the context of STGD1. These findings redefine the role of RIPK3 in retinal degeneration and emphasize the contextual plasticity of cell death regulators in neurodegenerative diseases.

neuroscience↗

bioRxiv2025

Spatial Transcriptomics Reveal Developmental Dynamics of the Human Cerebral Cortex and Striatum

The human fetal brain undergoes morphological changes that contribute to the development of regional functionalities. However, the features of structural development, the underlying molecular and cellular signatures in the fetal brain remain unclear. With spatial transcriptomics and snRNA-seq, we identified 25 forebrain regions and characterized the dynamic changes in the cortex and striatum during the late first and early second trimesters. In particular, we discovered that temporal lobe enriched NPY-expressing L2/3 EX neuron potentially interacted with L4 EX neurons during cortical expansion and arealization. Additionally, the gyrus and sulcus were developmental asynchronous, in which HOPX and SPARC genes were potentially involved. Further investigation on the striatum showed specific genes and cell types that enriched in patch and matrix compartments, and SST-positive interneurons potentially involved in the development of these structures. Together, our results give insights into the understanding of early fetal brain development.

bioinformatics↗

bioRxiv2025

LPS/TLR4-Activating Exosomes from M1-Polarized Avian Macrophages Enhances IBV Vaccine-Induced Protective Immunity in Chickens

Infectious bronchitis virus (IBV) presents a substantial economic burden to poultry production due to extensive serotypic diversity and limited cross-protection afforded by conventional vaccines. This study evaluated exosomes derived from M1-polarized chicken macrophages (HD11M1-exo) as a novel adjuvant for IBV vaccination. HD11M1-exo, isolated from LPS-activated HD11 macrophages via ultracentrifugation, demonstrated significant immunomodulatory properties across multiple experimental systems. In vitro analyses revealed HD11M1-exo enhanced macrophage phagocytosis and cellular immune activation via the LPS/TLR4 signaling pathway. In embryonated eggs, HD11M1-exo pre-treatment induced TNF- upregulation, enhanced viral resistance, and reduced pathological damage. In chickens, HD11M1-exo administration elevated CD80/CD86 and TGF-{beta}4 expression in respiratory tissues and increased secretory IgA in lacrimal fluid. When combined with H120 vaccine, HD11M1-exo significantly augmented both humoral immunity (elevated serum IgY and mucosal IgA) and cellular responses (increased CD80/CD86 expression), surpassing commercial adjuvants in efficacy. Following viral challenge, HD11M1-exo+H120 immunized chickens exhibited significantly reduced viral loads and attenuated histopathology compared to controls. These data collectively suggest that exosome-based formulations may serve as effective adjuvants for enhancing poultry vaccine immunogenicity and protective efficacy.

immunology↗

bioRxiv2021

Non-lesional and Lesional Lupus Skin Share Inflammatory Phenotypes that Drive Activation of CD16+ Dendritic Cells

Cutaneous lupus erythematosus (CLE) is a disfiguring and poorly understood condition frequently associated with systemic lupus. Studies to date suggest that non-lesional keratinocytes play a role in disease predisposition, but this has not been investigated in a comprehensive manner or in the context of other cell populations. To investigate CLE immunopathogenesis, normal-appearing skin, lesional skin, and circulating immune cells from lupus patients were analyzed via integrated single-cell RNA-sequencing and spatial-seq. We demonstrate that normal-appearing skin of lupus patients represents a type I interferon-rich, prelesional environment that skews gene transcription in all major skin cell types and dramatically distorts cell-cell communication. Further, we show that lupus-enriched CD16+ dendritic cells undergo robust interferon education in the skin, thereby gaining pro-inflammatory phenotypes. Together, our data provide a comprehensive characterization of lesional and non-lesional skin in lupus and identify a role for skin education of CD16+ dendritic cells in CLE pathogenesis.

immunology↗

bioRxiv2020

Phylogeny of the species-rich Pilea Lindl. (Urticaceae) supports its revised delimitation and infrageneric classification, including the resurrection of Achudemia Blume

ABSTRACTPilea Lindl., with 933 published names is the largest genus within the Urticaceae. Pilea was last monographed in 1869 and whilst the monophyly of the genus has been proposed by previous authors, this has been based on incomplete taxon sampling and the failure to resolve the position of key taxa. We aimed to generate a robust phylogeny for Pilea and allied genera that could provide a framework for testing the monophyly of Pilea, revising its delimitation and for answering broader scientific questions about this species-rich genus. To do so, we sought to sample taxa representative of previous infrageneric classifications and with anomalous inflorescences or flower configurations and to use the resulting phylogeny to evaluate the delimitation of Pilea and to establish an infrageneric classification. In addition, we included a representative of the Polynesian genus Haroldiella which, morphologically, is very similar to Pilea. Using Sanger sequence data from two plastid and one nuclear regions we constructed a phylogeny using Bayesian Inference, Maximum Likelihood and Maximum Parsiomony approaches. We used our phylogeny to evaluate the informativness of 19 morphological traits and applied both to delimit a monophyletic genus and infrageneric sections. Our results recovered Pilea as paraphyletic with respect to Lecanthus, a consequence of the recovery of a monophyletic clade comprising sections Achudemia and Smithiella, neither of which had been adequately sampled in previous studies. We also recovered Pilea as polyphyletic with respect to Haroldiella. We identified isomery between male and female flowers, flower part number and male sepal arrangement as being phylogenetically informative traits that can be used to delimit two genera, Achudemia, including section Smithiella, recovered as sister to Lecanthus, and Pilea, including Haroldiella, recovered as sister to both. On the basis of our evaluation of both morphological traits and phylogenetic relationships we propose a new infrageneric classification for the genus comprising seven sections, five of which we describe for the first time, § Trimeris Y.G.Wei & A.K.Monro, § Lecanthoides C.J.Chen, § Angulata L.F.Fu & Y.G.Wei, § Tetrameris C.J.Chen, § Verrucosa L.F.Fu & Y.G.Wei, § Plataniflora L.F.Fu & Y.G.Wei and § Leiocarpa L.F.Fu & Y.G.Wei. We also identify a trend of decreasing merism and fruit size, and increasing species-richness as Pilea diverges. In addition, we recover strong geographical structure within our phylogeny, sufficient to propose that Pilea originated in the IndoMalaya biogeographic domain.Competing Interest StatementThe authors have declared no competing interest.View Full Text

plant biology↗

bioRxiv2017

Interferon Regulatory Factor 5 (IRF5) Interacts with the Translation Initiation Complex and Promotes mRNA Translation During the Integrated Stress Response to Amino Acid Deprivation

Interferon Regulatory Factor 5 (IRF5) plays an important role in limiting pathogenic infection and tumor development. Host protection by IRF5 can occur through a variety of mechanisms including production of type I interferon and cytokines as well as the regulation of cell survival, growth, proliferation, and differentiation. While modulation of these cellular processes is attributed to IRF5 transcription factor function in the nucleus, emerging evidence suggests that IRF5 may also retain non-transcriptional regulatory properties within the cytoplasmic compartment. Consistent with this notion, we report the ability of IRF5 to control gene expression at the level of mRNA translation. Our findings demonstrate that IRF5 interacts with the translation initiation complex in the absence of the m7GTP cap-binding protein, eIF4E. We observed that under nutrient deprivation-induced cell stress, IRF5 promoted mRNA translation of the master integrated stress response (ISR) regulator, Activating Transcription Factor 4 (ATF4). Enhanced ATF4 protein expression correlated with increased levels of downstream target genes including CHOP and GADD34 and was associated with amplification of eIF2 de-phosphorylation and translational de-repression under stress. The novel mechanism we describe broadens our understanding of how IRF5 regulates gene expression and may govern diverse cellular processes in the absence of stimuli that trigger IRF5 nuclear translocation.

biochemistry↗