生命科学最新文献

Calcium signaling plays an essential role in integrating plant responses to diverse stimuli and regulating growth and development. While some signaling components and their roles are well-established, such as the ubiquitous calmodulin (CaM) sensor, plants possess a broader repertoire of calcium sensors. Notably, CaM-like proteins (CMLs) represent a poorly characterized class for which interacting partners and biological functions remain largely elusive. Our work investigates the role of Arabidopsis thaliana CML8 that exhibits a unique expression profile in seedlings. A reverse genetic approach revealed a function of CML8 in regulating root growth and hypocotyl elongation. RNA-seq analyses highlighted CML8 association with the regulation of numerous genes involved in growth and brassinosteroid (BR) signaling. Using co-immunoprecipitation experiments, we demonstrated that CML8 interacts with the BR receptor, BRI1, in planta in a ligand-dependent manner. This finding suggests the existence of a novel regulatory step in the BR pathway, involving calcium signaling.

Vascular plant one-zinc finger (VOZ) transcription factors (TFs) play crucial roles in plant immunity. Nevertheless, how VOZs modulate defense signaling in response to elicitor-induced resistance is not fully understood. Here, the defense elicitor β-aminobutyric acid (BABA) resulted in the visible suppression of Rhizopus rot disease of peach fruit caused by Rhizopus stolonifer. Defense priming by BABA was notably associated with increased levels of salicylic acid (SA) and SA-dependent gene expression. Data-independent acquisition proteomic analysis revealed that two VOZ proteins (PpVOZ1 and PpVOZ2) were substantially upregulated in BABA-induced resistance (BABA-IR). Furthermore, the interaction of PpVOZ1 and PpVOZ2 and their potential target of the TEOSINTE-BRANCHED1/CYCLOIDEA/PCF (TCP)-family protein PpTCP2 screened from protein-protein interaction networks was confirmed by yeast two-hybrid (Y2H), luciferase complementation imaging and glutathione S-transferase pull-down assays. Furthermore, subcellular localization, yeast one-hybrid, electrophoretic mobility shift assay and dual-luciferase reporter assays demonstrated that nuclear localization of both PpVOZ1 and PpVOZ2 was critical for their contribution to BABA-IR, as these proteins potentiated the PpTCP2-mediated transcriptional activation of isochorismate synthase genes (ICS1/2). The overexpression of both PpVOZ1 and PpVOZ2 could activate the transcription of SA-dependent genes and provide disease resistance in transgenic Arabidopsis. In contrast, the ppvoz1^cas9 and ppvoz2^cas9 loss-of-function mutations and the voz1^cas9 voz2^cas9 double mutation attenuated BABA-IR against R. stolonifer. Therefore, the three identified positive TFs, PpVOZ1, PpVOZ2, and PpTCP2, synergistically contribute to the BABA-activated priming of systemic acquired resistance in postharvest peach fruit by a VOZ-TCP-ICS regulatory module.

DNA, is assaulted by endogenous and exogenous agents that lead to the formation of damage. In order to maintain genome integrity DNA repair pathways must be efficiently activated to prevent mutations and deleterious chromosomal rearrangements. Conversely, genome rearrangement is also necessary to allow genetic diversity and evolution. The antagonist interaction between maintenance of genome integrity and rearrangements determines genome shape and organization. Therefore, it is of great interest to understand how the whole linear genome structure behaves upon formation and repair of DNA damage. For this, we used long reads sequencing technology to identify and to characterize genomic structural variations (SV) of wild-type Arabidopsis thaliana somatic cells exposed either to UV-B, to UV-C or to protons irradiations. We found that genomic regions located in heterochromatin are more prone to form SVs than those located in euchromatin, highlighting that genome stability differs along the chromosome. This holds true in Arabidopsis plants deficient for the expression of master regulators of the DNA damage response (DDR), ATM (Ataxia-telangiectasia-mutated) and ATR (Ataxia-telangiectasia-mutated and Rad3-related), suggesting that independent and alternative surveillance processes exist to maintain integrity in genic regions. Finally, the analysis of the radiations-induced deleted regions allowed determining that exposure to UV-B, UV-C and protons induced the microhomology-mediated end joining mechanism (MMEJ) and that both ATM and ATR repress this repair pathway.

Food security is increasingly threatened by climate change and environmental pressures that hinder plant growth and development. Harnessing soil microorganisms, such as mycorrhizal fungi and plant growth-promoting bacteria, offers a promising approach to boost crop production. However, existing screening methods for these microorganisms often prove ineffective in real-world, stress-prone environments, limiting the efficacy of microbial biofertilizers. To address this challenge, this review proposes the integration of silicon-renowned for its stress-mitigating properties in plants-with biofertilizers. Silicon has been shown to work synergistically with plant growth-promoting microorganisms, enhancing plant resilience to environmental stress while improving colonization efficiency and plant-microbe interactions in stressful conditions. By combining silicon with biofertilizers to create silicon-enriched biofertilizers, this strategy has the potential to optimize microbial performance and fortify food security against global challenges. The review advocates for the co-application of silicon and microbial biofertilizers as a sustainable solution to boost plant resilience against environmental stressors, thereby contributing to agricultural sustainability.

Lamiales is one of the largest orders of angiosperms with a complex evolutionary history and plays a significant role in human life. However, the polyploidization and chromosome evolution histories within this group remain in mystery. Among Lamiales, Isodon serra (Maxim.) Kudô shines for its abundance of diterpenes, notably tanshinones, long used in East Asia to combat toxicity and inflammation. Yet, the genes driving its biosynthesis and the factors governing its regulation linger in obscurity. Here, we present the telomere-to-telomere genome assembly of I. serra and, through gene-to-metabolite network analyses, pinpoint the pivotal tanshinone biosynthesis genes and their co-expressed transcription factors. Particularly, through luciferase (LUC) assays, we speculate that IsMYB-13 and IsbHLH-8 may upregulate IsCYP76AH101, which is the key step in the biosynthesis of the tanshinone precursor. Among Lamiales, Oleaceae, Gesneriaceae and Plantaginaceae successively sister to a clade of seven Lamiales families, all sharing a recent whole-genome duplication (designated as α event). By reconstructing the ancestral Lamiales karyotypes (ALK) and post-α event (ALKα), we trace chromosomal evolution trajectories across Lamiales species. Notably, one chromosomal fusion is detected from ALK to ALKα, and three shared chromosomal fusion events are detected sequentially from ALKα to I. serra, which fully supports the phylogeny constructed using single-copy genes. This comprehensive study illuminates the genome evolution and chromosomal dynamics of Lamiales, further enhancing our understanding of the biosynthetic mechanisms underlying the medicinal properties of I. serra.

Drought is a major abiotic stress that severely affects cereal production worldwide. Although several genes have been identified that enhance the ability of rice to withstand drought stress, further research is needed to fully understand the molecular mechanisms underlying the response to drought stress. Our study showed that overexpression of rice DNA binding with one finger 12 (OsDof12) enhances tolerance to drought stress. Rice plants overexpressing OsDof12 (OsDof12-OE) displayed significantly higher tolerance to drought stress than the parental japonica rice "Dongjin". Transcriptome analysis revealed that many genes involved in phenylpropanoid biosynthesis were upregulated in OsDof12-OE plants, including phenylalanine ammonia-lyase 4 (OsPAL4), OsPAL6, cinnamyl alcohol dehydrogenase 6 (CAD6), and 4-coumarate-coA ligase like 6 (4CLL6). Accordingly, this transcriptional alteration led to the substantial accumulation of phenolic compounds, such as sinapic acids, in the leaves of OsDof12-OE plants, effectively lowering the levels of reactive oxygen species. Notably, OsDof12 bound to the AAAG-rich core sequence of the OsPAL4 promoter and promoted transcription. In addition, GIGANTEA (OsGI) interacts with OsDof12 in the nucleus and attenuates the transactivation activity of OsDof12 on OsPAL4. Our findings reveal a novel role for OsDof12 in promoting phenylpropanoid-mediated tolerance to drought stress.

Because plants are immobile, they have developed intricate mechanisms to sense and absorb nutrients, adjusting their growth and development accordingly. Sulfur is an essential macroelement, but our understanding of its metabolism and homeostasis is limited. LSU (RESPONSE TO LOW SULFUR) proteins are plant-specific proteins with unknown molecular functions and were first identified during transcriptomic studies on sulfur deficiency in Arabidopsis. These proteins are crucial hubs that integrate environmental signals and are involved in the response to various stressors. Herein, we report the direct involvement of LSU proteins in primary sulfur metabolism. Our findings revealed that the quadruple lsu mutant, q-lsu-KO, which was grown under nonlimiting sulfate conditions, exhibited a molecular response resembling that of sulfur-deficient wild-type plants. This led us to explore the interactions of LSU proteins with sulfate reduction pathway enzymes. We found that all LSU proteins interact with ATPS1 and ATPS3 isoforms of ATP sulfurylase, all three isoforms of adenosine 5´ phosphosulfate reductase (APR), and sulfite reductase (SiR). Additionally, in vitro assays revealed that LSU1 enhances the enzymatic activity of SiR. These results highlight the supportive role of LSU proteins in the sulfate reduction pathway.

Human Snk is an evolutionarily conserved serine/threonine kinase essential for the maintenance of endocrine stability. The protein consists of a N-terminal catalytic domain and a C-terminal polo-box domain (PBD) that determines subcellular localization and substrate specificity. Here, an integrated strategy is described to explore the vast structural diversity space of Snk PBD-binding phosphopeptides at a molecular level using machine learning modeling, annealing optimization, dynamics simulation, and energetics rescoring, focusing on the recognition specificity and motif preference of the Snk PBD domain. We further performed a systematic rational design of potent phosphopeptide ligands for the domain based on the harvested knowledge, from which a few potent binders were also confirmed by fluorescence-based assays. A phosphopeptide PP17 was designed as a good binder with affinity improvement by 6.7-fold relative to the control PP0, while the other three designed phosphopeptides PP7, PP13, and PP15 exhibit a comparable potency with PP0. In addition, a basic recognition motif that divides potent Snk PBD-binding sequences into four residue blocks was defined, namely [Χ_-5Χ-₄]_block1-[Ω_-3Ω_-2Ω_-1]_block2-[pS₀/pT₀]_block3-[Ψ₊₁]_block4, where the X represents any amino acid, Ω indicates polar amino acid, Ψ denotes hydrophobic amino acid, and pS₀/pT₀ is the anchor phosphoserine/phosphothreonine at reference residue position 0.

The α_Lβ₂ integrin LFA-1 plays a key role in T-cell adhesion to the endothelial vasculature and migration into both secondary lymphoid organs and peripheral tissues via interactions with its target protein ICAM-1, but the pathways that regulate LFA-1-mediated T-cell polarity and migration are not fully understood. In this study we screened two RNAi libraries targeting G protein-coupled receptors (GPCR)/GPCR-associated proteins and kinases in a HuT 78 T cell line model of LFA-1-stimulated T-cell migration. Based on staining of the actin cytoskeleton, multiple parameters to measure cell morphology were used to assess the contribution of 1109 genes to LFA-1-mediated T-cell polarity and migration. These RNAi screens identified a number of both novel and previously identified genes that either increased or decreased the polarity and migratory capacity of these cells. Following multiparametric analysis, hierarchical clustering and pathway analysis, three of these genes were characterized in further detail using primary human T cells, revealing novel roles for the heterotrimeric G protein subunit Gβ1 and Casein Kinase 2 in LFA-1-mediated T-cell polarity and migration in vitro. Our studies also highlighted a new role for ICAP-1, an adaptor protein previously described to be associated with β1 integrins, in β2 integrin LFA-1-directed migration in T cells. Knockdown of ICAP-1 expression in primary T cells revealed a role in cell polarity, cell velocity and transmigration towards SDF-1 for this adaptor protein. This study therefore uncovers new roles for GPCR/GPCR-associated proteins and kinases in T-cell migration and provides potential novel targets for modulation of the T-cell immune response.

T cells of the adaptive immune system recognize pathogens and malignantly transformed cells through a process called antigen presentation. During this process, peptides are displayed on major histocompatibility complex (MHC) class I and II molecules. Self-reactive T cells are typically removed or suppressed during T-cell development and through peripheral tolerance mechanisms, ensuring that only T cells recognizing peptides that are either absent or present in low abundance under normal conditions remain. This selective process allows T cells to respond to peptides derived from foreign proteins while ignoring those from self-proteins. However, T cells can also respond to peptides derived from proteins that have undergone post-translational modifications (PTMs). Over 200 different PTMs have been described, and while they are essential for protein function, localization and stability, their dysregulation is often associated with disease conditions. PTMs can affect the proteolytic processing of proteins and prevent MHC binding, thereby changing the repertoire of peptides presented on MHC molecules. However, it is also increasingly evident that many peptides presented on MHC molecules carry PTMs, which can alter their immunogenicity. As a result, the presentation of post-translationally modified peptides by MHC molecules plays a significant role in various diseases, as well as autoimmune disorders and allergies. This review will provide an overview of the impact of PTMs on antigen presentation and their implications for immune recognition and disease.