生命科学最新文献

Red blood cells (RBC, erythrocytes) are the main cell population that ensures tissue oxygenation and forms the ordered movement of all blood cells through the vessels. Disturbances in the physiological deformability of red blood cells aggravate the degree of anemia in two ways: aberrant red blood cells are rapidly eliminated by sequestration and destruction in the spleen and liver; and second, poorly deformable red blood cells have a reduced potential for gas exchange in the capillaries due to a decrease in the membrane contact area. Regardless of the etiology of hepatosis, liver cirrhosis (LC) develops persistent anemia, but disorders of erythrocyte deformability in patients with decompensated liver cirrhosis have been poorly studied. Using laser diffraction, flow cytometry, and microfluidic analysis, we showed that erythrocytes of LC patients develop disorders of deformability caused by the stress type of erythropoiesis (release of immature reticulocytes into circulation, an increase in the proportion of phosphatidylserine-presenting erythrocytes, a decrease in the activity of cytosolic esterases. In LC, erythrocytes have a pronounced rigidity to hypoosmotic load: induced hemolysis is incomplete, its speed is reduced, which indicates a decrease in the deformability of erythrocytes. Deformability disorders affected the ability of erythrocytes to pass through microchannels - the transit velocity was decreased, a high percentage of occlusions was observed, i.e., signs of microrheology disorders were identified. A connection was established between the disorders of erythrocyte microrheology depending on the degree of LC progression.

This study characterizes extracellular vesicles (EVs) produced by multipotent mesenchymal stromal cells (MMSCs) in culture medium. The vesicles isolated by centrifugation contained proteins specific to exosomes and had a characteristic size. The effects of vesicles produced by MMSC (MMSC-EVs) on kidney cells under normal and pathological conditions were analyzed. MMSC-EVs increased the proliferation rate of renal epithelial cells after damage caused by oxygen-glucose deprivation. The microRNA expression profile in MMSC-EVs showed that both damage-aggravating and protective microRNAs were highly expressed in them. The overall effect of MMSC-EVs on kidney cells appears to result from the complex interactions of protein signals and the regulatory effects of microRNAs.

Plant nuclear genomes contain a variable, though typically minor, fraction of DNA sequences of plastid origin known as NUPTs. Unlike the massive transfer of DNA and genes from the proto-organelle genome to the nucleus that occurred during the endosymbiotic event that gave rise to plastids, the formation of NUPTs is an ongoing process that does not imply concomitant DNA loss. Although NUPTs are generally considered to be potentially deleterious insertions that are continuously generated and rapidly eliminated at near-constant turnover rates, accumulating evidence reveals alternative evolutionary trajectories. In this review, we discuss recent findings that highlight the episodic formation of NUPTs, their subsequent proliferation, and their eventual long-term fixation within the nuclear genome. We also explore their non-random spatial association with specific genomic elements. NUPTs show preferential overlap with specific superfamilies of transposable elements, which may facilitate their proliferation and dispersal throughout the nuclear genome. Regarding protein-coding genes, the contribution of NUPTs varies among species. In contrast, NUPTs are found to be consistently enriched among certain classes of non-coding RNA genes, notably rRNA, tRNA, and specific regulatory RNA families, suggesting that they are involved in the evolution of gene regulation and translational machinery. Overall, these findings underscore the unexpected complexity of the mechanisms underlying NUPT formation and support the idea that they are a significant source of genome variation and evolutionary innovation. Further research is necessary to fully elucidate the mechanisms underlying NUPT formation, as well as to determine their potential adaptive significance in plant genome evolution.

Labor-saving and high-light-efficiency tree architecture is a key breeding objective for woody fruit trees like citrus. However, population genetics information on these traits remains limited. In this study, tree architecture, thorn, and leaf traits were evaluated in 353 F₂ progeny derived from a cross between Clementine mandarin and precocious trifoliate orange-an early-flowering variety. A random subset of 300 offspring was sequenced for a genome-wide association study (GWAS), which detected 10 216 significantly associated SNPs and defined several major quantitative trait loci (QTLs) for the target traits. Subsequent bulked segregant analysis (BSA) and GWAS on individuals with extreme compound leaf phenotypes mapped the causal gene(s) to a 0.8 Mb region (22.15-22.95 Mb) on chromosome 4. Genetic analysis across multiple hybrid combinations confirmed that the compound leaf trait in trifoliate orange is dominantly inherited and follows Mendelian segregation. Transcriptome profiling of parental leaves at different developmental stages identified a KNOX gene, CiKNAT6, as a candidate. Further validation using CAPS markers and Hi-Tom sequencing demonstrated tight linkage between an InDel polymorphism in CiKNAT6 and leaf shape across diverse citrus species and the F₂ population, with co-segregation observed for the compound leaf trait. Due to alternative splicing producing seven splice variants, the CiKNAT6 DNA sequence was selected for genetic transformation experiments. Functional analysis revealed that the Clementine mandarin allele of CiKNAT6 is non-functional owing to an InDel, whereas ectopic expression of the trifoliate orange allele in tobacco and lemon induced leaf curling and reduced leaf size. CRISPR-Cas9 knockout of CiKNAT6 in trifoliate orange resulted in increased leaf area. These findings provide valuable genetic resources and insights for future studies on tree architecture and leaf morphology.

The Mediator complex interacts with transcription factors to guide the assembly of the Pre-initiation complex in promoter DNA. It also interacts with hormone signaling components, connecting hormone signaling to gene expression, serving as a hub for signal integration. Despite its role being essential, some Mediator subunits have specific roles. Here, we characterized the role of the MED3 subunit of Arabidopsis thaliana. We obtained null med3 mutants by CRISPR Cas9 and show that MED3 promotes flowering in a photoperiod and temperature independent manner. med3 mutants behave similarly to autonomous pathway mutants and we show that late flowering is due to high expression of FLOWERING LOCUS C. However, we also show that exogenous application of gibberellic acid (GA) to med3 mutants drastically changes its architecture, leading to a disproportionately higher number of cauline leaves with respect to rosette leaves. These findings suggest that GAs more effectively promote bolting of med3 mutants, but delay flower appearance later, suggesting that med3 mutants are more sensitive to GAs during reproductive development. Finally, we obtained transcriptomic data showing that ABA response genes are expressed at lower levels in med3 mutants, and show that med3 mutants are less sensitive to ABA during germination. Given the antagonistic roles of GA and ABA, MED3 may also have a role in balancing the relative sensitivity to these hormones.

Nitric oxide (NO) inhibits climacteric fruit ripening, but its mechanisms remain elusive. Here, S-nitrosoglutathione (GSNO, a NO donor) reduces carotenoid accumulation in tomato fruit, confirming NO's role as carotenoid biosynthesis suppressor. Transcriptome analysis identified SlSPL10 (SQUAMOSA promoter binding protein-like 10) as a key player during this process. Genetic evidence further revealed that SlSPL10 negatively regulates carotenoid synthesis. Moreover, GSNO fails to suppress carotenoid synthesis in slspl10 mutant fruit, in contrast to wild-type fruit, highlighting the involvement of SlSPL10 in NO-inhibited carotenoid synthesis. Transcriptomic profiling of slspl10 mutant fruit showed that both NO and SlSPL10 regulate key carotenoid synthesis genes (SlGPS, SlPDS, SlZDS, SlZISO, and SlCRTISO). SlSPL10 directly binds to the promoters of these genes to repress their transcription, and NO enhances the transcriptional inhibition of SlGPS, SlZISO, and SlCRTISO. These three genes are indispensable for SlSPL10's role in NO-mediated carotenoid suppression. Collectively, NO enhances SlSPL10-mediated repression of carotenoid biosynthesis gene expression, reducing carotenoid accumulation in tomato fruit.

The root system is pivotal for plant development, enabling both vegetative growth and tolerance to abiotic stresses like salinity. However, the molecular mechanisms governing root adaptive development in response to salt stress remain poorly understood in apple (Malus domestica Borkh.). In this study, we identified the salt stress-responsive WRKY transcription factor MdWRKY75. Overexpression of MdWRKY75 in transgenic apple negatively regulates adventitious root (AR) formation and salt stress tolerance, whereas reducing MdWRKY75 expression yields the opposite phenotype. Moreover, MdWRKY75 directly binds to the promoter of MdSAUR15 (SMALL AUXIN UP RNA15) and transcriptionally represses the expression of MdSAUR15, which, when overexpressed, promotes AR formation and enhances salt stress tolerance. We further demonstrated that MdWRKY75 interacts with MdWOX11, a WUSCHEL-related homeobox (WOX) transcription factor, both in vitro and in vivo. MdWOX11 expression is upregulated and enhances AR formation under salt stress. Additionally, MdWOX11 reduces the binding of MdWRKY75 to the MdSAUR15 promoter, and alleviates the MdWRKY75-mediated inhibitory effect on MdSAUR15 expression. Collectively, our study provides a MdWOX11-MdWRKY75-MdSAUR15 module regulating root adaptation in response to salt stress in apple.