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Liang Liu

Publications and source records attributed to Liang Liu.

6 recordsLinked to original sources
PubMed2026

Long-term saline-alkaline selection rewires the growth-survival trade-off in Priestia megaterium.

Saline-alkaline soils impose persistent osmotic, ionic, pH, and nutrient stress on soil microorganisms, but the evolutionary routes by which beneficial bacteria adapt to such conditions remain poorly resolved. We performed adaptive laboratory evolution to examine the adaption of the plant growth-promoting rhizobacterium Priestia megaterium HA22 to long-term oligotrophic saline-alkaline selection. After 175 serial transfers, the evolved lineage proliferated stably at 40 g L-1 Na2SO4 at pH 10.0, whereas the wild-type strain failed to proliferate. Genome resequencing and allelic replacement revealed a 5-bp insertion in spo0A, the master sporulation regulator, as a major adaptive mutation. This mutation abolished sporulation; shortened the lag phase; and enhanced vegetative growth, nutrient uptake, and expression of tricarboxylic acid cycle and nitrogen metabolism gene under saline-alkaline stress. According to untargeted metabolomics, adaptation was accompanied by increased amino acid metabolism and aminoacyl-tRNA biosynthesis, with proline, isoleucine and pantothenic acid functionally promoting growth. A point mutation in ugpB enhanced glycerol-3-phosphate uptake, increased peptidoglycan and wall teichoic acid levels, and partially rescued the survival cost of the spo0A mutation. In greenhouse assays under combined saline-alkaline stress, the evolved strain increased soybean shoot dry weight and root dry weight by 56.08% and 27.02%, respectively. These results indicate that prolonged, predictable saline-alkaline selection can favor active growth rather than dormancy when compensatory cell envelope reinforcement buffers survival costs.

Adaptive laboratory evolution↗
PubMed2026

The complete chloroplast genome sequence and phylogenetic position of Mallotus apelta.

Mallotus apelta is a perennial species of Euphorbiaceae widely distributed in subtropical East and Southeast Asia. In this study, we sequenced and analyzed its complete chloroplast genome. The genome was 164,055 bp in length and exhibited a typical quadripartite structure, comprising an LSC region of 88,899 bp, an SSC region of 18,494 bp, and two IR regions of 28,331 bp each. A total of 124 genes were annotated. Comparative analyses revealed conserved genome organization and IR boundaries among Mallotus species. Phylogenetic analysis showed that M. apelta was closely related to M. paniculatus, providing valuable resources for Mallotus phylogenetic studies.

Euphorbiaceae↗
PubMed2026

Single-cell transcriptomics reveals heterogeneous stress responses and Mg2+-mediated survival mechanisms in Lactobacillus delbrueckii subsp. bulgaricus during freeze-drying and storage.

Maintaining the viability of lactic acid bacteria during dehydration and subsequent storage remains a significant challenge. Here, we employed single-cell RNA sequencing to reveal the heterogeneous stress responses of Lactobacillus delbrueckii subsp. bulgaricus, identifying seven distinct transcriptional clusters across the liquid culture, freeze-drying, and storage phases. The dominant clusters in the freeze-drying and storage were not completely consistent, showing significant functional differentiation. Genomic stability may be important for survival during freeze-drying and storage, while intracellular energy homeostasis appears important for viability during storage. The magnesium transporter mgtB was highly expressed in clusters tolerant to freeze-drying and storage, suggesting a critical role for Mg2+ homeostasis. Further experimental validation confirmed that Mg2+ treatment significantly bolstered stress resistance, increasing immediate post-freeze-drying survival by over 2-fold (up to 92.90%) and post-storage survival by over 5-fold (up to 5.98%). Proteomic data indicated that Mg2+ supplementation correlated with the maintenance of several biological functions potentially relevant to bacterial survival during freeze-drying and storage, including DNA repair, translation, and central carbon metabolism. These findings provide a map of microbial stress resistance through population heterogeneity and offer a potential strategy that may be adapted for enhancing the stability of other industrial lactic acid bacteria products.

Freeze Drying↗
PubMed2026

Enhanced HIF-1α cooperation by a human RORγt mutant potentiates Th17 pathogenicity.

T helper 17 (Th17) cells are pivotal in mucosal defense and autoimmune pathology, with their function governed by the transcription factor retinoic acid receptor-related orphan receptor gamma t (RORγt). Although genome-wide association studies link RORC variants to inflammatory diseases, their functional consequences remain poorly understood. We identify a pathogenic RORγt mutation N277D (mouse homolog N275D) that amplifies Th17 pathogenicity through cooperation with hypoxia-inducible factor HIF-1α. This mutation enhances IFN-γ and other Th1-type cytokine production by Th17 cells, exacerbating colitis without disrupting T cell development or homeostasis. Integrated transcriptomic and metabolomic profiling reveals activation of glycolytic and hypoxia-associated pathways, consistent with increased RORγtN275D recruitment by HIF-1α to the Pdk1 locus. Notably, silencing Pdk1 normalizes the excessive IFN-γ production in RORγtN275D Th17 cells. Together, these findings define a regulatory axis linking RORγt and HIF-1α that coordinates transcriptional and metabolic programs in pathogenic Th17 cells, providing a framework for dissecting the functional impact of autoimmune risk variants.

CP: immunology↗
PubMed2026

Targeting STK17B kinase activates ferroptosis and suppresses drug resistance in multiple myeloma.

The progression of multiple myeloma (MM), an incurable malignancy of plasma cells, is often associated with the suppression of ferroptosis, a type of cell death driven by iron-dependent lipid peroxidation. The mechanisms underlying this suppression remain largely unknown. Here, we identified serine/threonine kinase 17b (STK17B) kinase as a critical suppressor of ferroptosis in MM. Elevated levels of STK17B are associated with poor overall survival in patients with MM, and STK17B expression is significantly higher in relapsed vs newly diagnosed MM cases. We found that inhibiting STK17B in MM cells increased the labile iron pool, enhanced lipid peroxidation, and sensitized cells to conventional anti-MM therapies. Notably, an orally available, in-house-generated STK17B inhibitor induced ferroptosis and significantly reduced tumor growth in MM xenograft mouse models. Mechanistically, proximity labeling assay combined with the phospho-proteomic analysis identified 2 major regulators of iron uptake and transport as direct targets of STK17B: iron-responsive element binding protein 2 (IREB2), and heat shock protein family B member 1 (HSPB1). We demonstrated that STK17B phosphorylates critical regulatory sites on IREB2 (S157) and HSPB1 (S15), thereby modulating the balance between IREB2 and HSPB1 downstream effectors, proferroptotic transferrin receptor, and antiferroptotic ferritin heavy chain proteins. Furthermore, we demonstrated that STK17B indirectly maintains activating phosphorylation of STAT3, a ferroptosis suppressor and a major driver of MM pathobiology. Our findings uncovered a clinically relevant and targetable STK17B-pIREB2S157/pHSPB1S15 signaling axis that suppresses ferroptosis and contributes to drug resistance in MM.

Ferroptosis↗
PubMed2024

Shared differential factors underlying individual spontaneous neural activity abnormalities in major depressive disorder.

BACKGROUND: In contemporary neuroimaging studies, it has been observed that patients with major depressive disorder (MDD) exhibit aberrant spontaneous neural activity, commonly quantified through the amplitude of low-frequency fluctuations (ALFF). However, the substantial individual heterogeneity among patients poses a challenge to reaching a unified conclusion. METHODS: To address this variability, our study adopts a novel framework to parse individualized ALFF abnormalities. We hypothesize that individualized ALFF abnormalities can be portrayed as a unique linear combination of shared differential factors. Our study involved two large multi-center datasets, comprising 2424 patients with MDD and 2183 healthy controls. In patients, individualized ALFF abnormalities were derived through normative modeling and further deconstructed into differential factors using non-negative matrix factorization. RESULTS: Two positive and two negative factors were identified. These factors were closely linked to clinical characteristics and explained group-level ALFF abnormalities in the two datasets. Moreover, these factors exhibited distinct associations with the distribution of neurotransmitter receptors/transporters, transcriptional profiles of inflammation-related genes, and connectome-informed epicenters, underscoring their neurobiological relevance. Additionally, factor compositions facilitated the identification of four distinct depressive subtypes, each characterized by unique abnormal ALFF patterns and clinical features. Importantly, these findings were successfully replicated in another dataset with different acquisition equipment, protocols, preprocessing strategies, and medication statuses, validating their robustness and generalizability. CONCLUSIONS: This research identifies shared differential factors underlying individual spontaneous neural activity abnormalities in MDD and contributes novel insights into the heterogeneity of spontaneous neural activity abnormalities in MDD.

Humans↗