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PubMed2026

Alleviation of CO2-Induced Reductions in Tomato Photosynthesis Under Deficit Irrigation by Purple Nonsulfur Photosynthetic Bacteria.

The stimulatory effect of elevated CO2 (eCO2) on photosynthesis in most C3 crops under water deficit often declines over time due to photosynthetic acclimation. An exception occurs in plants inoculated with symbiotic nitrogen-fixing bacteria. Photosynthetic bacteria (PSB), specifically anoxygenic purple nonsulfur bacteria (Rhodopseudomonas palustris in this study), a group of nitrogen-fixing bacteria, are effective in enhancing crop photosynthesis. Therefore, this study investigated the synergistic effects of PSB and eCO2 in alleviating the effects of deficit irrigation and enhancing photosynthetic capacity in tomato plants during prolonged exposure. Our results showed that photosynthetic efficiency was significantly reduced in noninoculated plants under eCO2, and this reduction was more pronounced under water deficit. Proteomic analysis revealed that in eCO2-treated plants, the downregulation of cell wall proteins increased mesophyll resistance to CO2 diffusion, while the suppression of the photosynthetic apparatus impaired electron transport capacity, ultimately reducing CO2 assimilation efficiency. In contrast, these negative effects were alleviated by PSB inoculation. PSB promoted the upregulation of proteins involved in photosynthesis under deficit irrigation, as well as proteins related to chlorophyll biosynthesis, components of photosystem I and II, and light-harvesting complex proteins. These proteins contributed to improved photosynthetic efficiency during deficit irrigation and photosynthetic acclimation. Physiological analyses further confirmed that PSB inoculation enhanced nitrogen content, electron transport capacity, chlorophyll biosynthesis, and overall photosynthetic performance under eCO2 and deficit irrigation, resulting in improved plant growth. These findings suggest that PSB inoculation is a promising strategy to sustain and enhance the CO2 fertilization effect on crop productivity under water-limited conditions.

Photosynthesis↗
PubMed2024

Expression pattern of Stlhcb gene family in potato and effects of overexpression of Stcp24 gene on potato photosynthesis.

Potato is one of the four staple food crops in the world. It has a wide range of cultivation, high yield, and high nutritional value. Enhancing the photosynthesis of potato is particularly important as it leads to an increase in the potato yield. The light-harvesting pigment-binding protein complex is very important for plant photosynthesis. We identified 12 Stlhcb gene family members from the potato variety "Atlantic" using transcriptome sequencing and bioinformatics. The proteins encoded by the Stlhcb gene family have between 3358 and 4852 atomic number, a relative molecular weight between 24060.16 and 34624.54 Da, and an isoelectric point between 4.99 and 8.65. The RT-qPCR results showed that the 12 Stlhcb genes were expressed in a tissue-specific and time-dependent fashion under low light. The relative expression of the Stlhcb genes in the leaves was significantly higher than that in the stems and roots, and the relative expression of these genes first increased and then decreased with the prolongation of light exposure time. The Stcp24 gene with the highest expression was cloned, and an expression vector was constructed. A subcellular localization analysis was performed in tobacco and an overexpression experiment was performed in potato using an Agrobacterium-mediated method. The subcellular localization analysis showed that the protein encoded by Stcp24 was located in chloroplasts as expected. Overexpression of Stcp24 in transgenic potato increased the yield of potatoes and the content of chlorophyll a and b; increased the net photosynthetic rate, transpiration rate, stomatal conductance, electron transport efficiency, and semi-saturated light intensity; and promoted photosynthesis and plant growth. This study provides a reference for the study of the function of the potato light-harvesting pigment-binding protein gene family. It lays a foundation for further study of the mechanism of the photosynthesis of potato, improvement of the light energy utilization of potato, and molecular breeding of potato.

Solanum tuberosum↗
PubMed2026

Mitochondrial integrated stress response activation creates a therapeutic vulnerability to MCL-1 inhibition in acute myeloid leukemia.

MCL-1 (myeloid cell leukemia-1) promotes survival and confers therapeutic resistance in acute myeloid leukemia (AML), particularly in high-risk subtypes harboring KMT2A rearrangements (KMT2A-r). Clinical trials involving patients with hematological malignancies treated with MCL-1 inhibitor monotherapy have been hampered by dose-limiting toxicity and poor response rates. Therefore, we sought to identify combinatorial treatment approaches to enhance the efficacy of MCL-1 inhibitors with the goal of improving response rates and limiting toxicities. Here, we report the inhibition of electron transport chain (ETC) complex I (CI) function as a synthetic lethal partner for MCL-1 inhibition. Co-targeting CI and MCL-1 synergistically reduces the viability in AML cell lines and patient-derived xenograft (PDX) samples in vitro, while significantly prolonging survival in mice bearing PDX AML, indicating the preclinical potential for this combinatorial therapy. These findings provide a mechanistic rationale and preclinical evidence for dual inhibition of MCL-1 and CI as a therapeutic strategy, offering a potential path to overcome resistance to single-agent MCL-1 inhibitors and improve outcomes for patients with high-risk AML. Mechanistically, we reveal that CI inhibition induces the activation of the integrated stress response, resulting in ATF4 activation downstream of the eIF2α kinase, HRI (Heme-regulated inhibitor). HRI activation via CI inhibition is dependent on the mitochondrial stress messenger, DELE1. Together, these results indicate that co-inhibition of MCL-1 and ETC CI function has the potential for improving responses in patients with KMT2A-r AML.

Humans↗
PubMed2026

IDH3-dependent mitochondrial function in stromal fibroblasts suppresses malignant tumor growth.

Malignant solid tumors comprise not only cancer cells but also diverse non-cancerous stromal cells that shape the tumor microenvironment. The tricarboxylic acid (TCA) cycle has an overarching presence in providing substrates needed to drive the electron transport chain and, ultimately, ATP synthesis. However, it remains unclear which stromal cell lineages influence tumor growth through TCA-dependent mitochondrial function, and whether such activities act in a tumor-promoting or tumor-suppressive manner. Isocitrate dehydrogenase 3 (IDH3), a rate-limiting TCA cycle enzyme that generates NADH to support mitochondrial respiration, provides a genetic entry point to interrogate mitochondrial TCA-dependent function in stromal cells. In this study, we established a mouse model in which tamoxifen administration induces CreERT2-dependent knockout of the α subunit of IDH3 (IDH3α) in all somatic cells. Using this model with transplantation of Idh3a-intact murine cancer cells, we found that host Idh3a deficiency accelerated growth of murine MC38 tumors in a cancer cell line-dependent manner. Bone marrow chimera experiments indicated that hematopoietic lineages were not responsible for this phenotype, suggesting a contribution from tissue-resident non-hematopoietic stromal cells that are not replaced by bone marrow transplantation. Single-cell RNA sequencing of human tumor specimens revealed broad IDH3A expression across multiple tumor microenvironment compartments, including fibroblasts. Consistently, in vitro co-culture assays demonstrated that Idh3a-intact, but not Idh3a-KO, fibroblasts suppressed cancer cell proliferation in a contact-dependent manner. Together, these findings identify IDH3α-dependent mitochondrial function in fibroblasts as a critical determinant of tumor progression and suggest that stromal mitochondrial metabolism represents an important axis for modulating tumor behavior.

Cancer↗
PubMed2025

Effects of nitrogen allocation and photosynthetic proteins response in peanut leaves on photosynthesis under conditions of water scarcity and nitrogen deficiency.

Leaf nitrogen allocation and photosynthetic proteins response can affect net photosynthetic rate (Pn), ultimately influencing crop yield under diverse environmental stresses. However, the internal relationship between Pn with leaf nitrogen allocation and photosynthetic proteins response under nitrogen or water scarcity in peanut (Arachis hypogaea L.) remains elusive. Here, comprehensive physiological property and proteomic analyses of peanut were conducted, revealing that both nitrogen and water scarcity remarkably impeded leaf growth and reduced Pn. Nitrogen deficiency significantly reduced the total nitrogen content per unit leaf area (Narea), chlorophyll content, and Pn, whereas drought stress caused a greater decline in photosynthetic nitrogen use efficiency (PNUE). The allocation of leaf nitrogen to photosynthetic components, including the carboxylation system and electron transport system in leaves, was significantly reduced when subjected to individual or combined deficiency. Proteomic analyses exhibited that several key photosynthetic proteins underwent a decrease under both single and combined water and nitrogen deficiency conditions. Thereby, Pn may decline due to the disruption of nitrogen allocation and down-regulated expression of photosynthetic proteins under these stress conditions. Our findings establish a benchmark for future research exploring the roles of leaf nitrogen allocation and photosynthetic proteins in the plant's response to nitrogen or water deficiency.

Nitrogen↗