Elevated CO Shifts Photosynthetic Constraint from Stomatal to Biochemical Limitations During Induction in and .

The relative impacts of biochemical and stomatal limitations on photosynthesis during photosynthetic induction have been well studied for diverse plants under ambient CO concentration (). However, a knowledge gap remains regarding how the various photosynthetic components limit duction efficiency under elevated CO. In this study, we experimentally investigated the influence of elevated CO (from 400 to 800 μmol mol) on photosynthetic induction dynamics and its associated limitation components in two broadleaved tree species, and .

The Immune Modulatory Role of TIF1 Proteins.

The function of immune cells is delicately regulated under a variety of molecular networks. Transcriptional intermediary factor 1 (TIF1) family proteins, consisting of TRIM24, TRIM28 and TRIM33, share a highly conserved RING domain that is essential for the regulation of protein ubiquitination functioning as E3 ubiquitin ligases. TIF1 family proteins are diversely expressed in different types of immune cells, and participate in the regulation of various of cellular functions including chromosome modification, DNA repair, tumor progression, and immunity.

Chemoradiotherapy-induced ACKR2 tumor cells drive CD8 T cell senescence and cervical cancer recurrence.

Tumor recurrence after chemoradiotherapy is challenging to overcome, and approaches to predict the recurrence remain elusive. Here, human cervical cancer tissues before and after concurrent chemoradiotherapy (CCRT) analyzed by single-cell RNA sequencing reveal that CCRT specifically promotes CD8 T cell senescence, driven by atypical chemokine receptor 2 (ACKR2) CCRT-resistant tumor cells. Mechanistically, ACKR2 expression is increased in response to CCRT and is also upregulated through the ligation of CC chemokines that are produced by activated myeloid and T cells.

Single-cell atlas reveals a distinct immune profile fostered by T cell-B cell crosstalk in triple negative breast cancer.

Background: Characterizing the unique immune microenvironment of each tumor is of great importance for better predicting prognosis and guiding cancer immunotherapy. However, the unique features of the immune microenvironment of triple negative breast cancer (TNBC) compared with other subtypes of breast cancer remain elusive. Therefore, we aimed to depict and compare the immune landscape among TNBC, human epidermal growth factor receptor 2-positive (HER2 ) breast cancer, and luminal-like breast cancer.

Biomarkers of aging.

Aging biomarkers are a combination of biological parameters to (i) assess age-related changes, (ii) track the physiological aging process, and (iii) predict the transition into a pathological status. Although a broad spectrum of aging biomarkers has been developed, their potential uses and limitations remain poorly characterized. An immediate goal of biomarkers is to help us answer the following three fundamental questions in aging research: How old are we? Why do we get old? And how can we age slower? This review aims to address this need.

Goliath induces inflammation in obese mice by linking fatty acid β-oxidation to glycolysis.

Obesity is associated with metabolic disorders and chronic inflammation. However, the obesity-associated metabolic contribution to inflammatory induction remains elusive. Here, we show that, compared with lean mice, CD4 T cells from obese mice exhibit elevated basal levels of fatty acid β-oxidation (FAO), which promote T cell glycolysis and thus hyperactivation, leading to enhanced induction of inflammation.

Ezh2 competes with p53 to license lncRNA Neat1 transcription for inflammasome activation.

Inflammasome contributes to the pathogenesis of various inflammatory diseases, but the epigenetic mechanism controlling its activation remains elusive. Here, we found that the histone methyltransferase Ezh2 mediates the activation of multiple types of inflammasomes in macrophages/microglia independent of its methyltransferase activity and thus promotes inflammasome-related pathologies. Mechanistically, Ezh2 functions through its SANT2 domain to maintain the enrichment of H3K27 acetylation in the promoter region of the long noncoding RNA (lncRNA) Neat1, thereby promoting chromatin accessibility and facilitating p65-mediated transcription of Neat1, which is a critical mediator of inflammasome assembly and activation.

E3 ligase MKRN3 is a tumor suppressor regulating PABPC1 ubiquitination in non-small cell lung cancer.

Central precocious puberty (CPP), largely caused by germline mutations in the MKRN3 gene, has been epidemiologically linked to cancers. MKRN3 is frequently mutated in non-small cell lung cancers (NSCLCs) with five cohorts. Genomic MKRN3 aberrations are significantly enriched in NSCLC samples harboring oncogenic KRAS mutations.

BFAR coordinates TGFβ signaling to modulate Th9-mediated cancer immunotherapy.

TGFβ is essential for the generation of anti-tumor Th9 cells; on the other hand, it causes resistance against anti-tumor immunity. Despite recent progress, the underlying mechanism reconciling the double-edged effect of TGFβ signaling in Th9-mediated cancer immunotherapy remains elusive. Here, we find that TGFβ-induced down-regulation of bifunctional apoptosis regulator (BFAR) represents the key mechanism preventing the sustained activation of TGFβ signaling and thus impairing Th9 inducibility.

Cytoplasmic DNA sensing by KU complex in aged CD4 T cell potentiates T cell activation and aging-related autoimmune inflammation.

Aging is associated with DNA accumulation and increased homeostatic proliferation of circulating T cells. Although these attributes are associated with aging-related autoimmunity, their direct contributions remain unclear. Conventionally, KU complex, the regulatory subunit of DNA-dependent protein kinase (DNA-PK), together with the catalytic subunit of DNA-PK (DNA-PKcs), mediates DNA damage repair in the nucleus.

TRIM24 facilitates antiviral immunity through mediating K63-linked TRAF3 ubiquitination.

Ubiquitination is an essential mechanism in the control of antiviral immunity upon virus infection. Here, we identify a series of ubiquitination-modulating enzymes that are modulated by vesicular stomatitis virus (VSV). Notably, TRIM24 is down-regulated through direct transcriptional suppression induced by VSV-activated IRF3.

Modulation of M2 macrophage polarization by the crosstalk between Stat6 and Trim24.

Stat6 is known to drive macrophage M2 polarization. However, how macrophage polarization is fine-tuned by Stat6 is poorly understood. Here, we find that Lys383 of Stat6 is acetylated by the acetyltransferase CREB-binding protein (CBP) during macrophage activation to suppress macrophage M2 polarization.

Intronic (TTTGA) insertion in SAMD12 also causes familial cortical myoclonic tremor with epilepsy.

Background: Intronic (TTTCA) insertions in the SAMD12, TNRC6A, and RAPGEF2 genes have been identified as causes of familial cortical myoclonic tremor with epilepsy.

Objective: To identify the cause of familial cortical myoclonic tremor with epilepsy pedigrees without (TTTCA) insertions in SAMD12, TNRC6A, and RAPGEF2.

Methods: Repeat-primed polymerase chain reaction, long-range polymerase chain reaction, and Sanger sequencing were performed to identify the existence of a novel (TTTGA) insertion.