Decapod iridovirus 1 (DIV1) poses a major challenge to sustainable shrimp farming and poses a serious hazard to aquaculture industry. This study investigated the complex interaction between DIV1 infection and water temperature, focusing on the effect of high temperature on DIV1 infection due to Penaeus monodon. Using models of latent and acute infection, the study revealed the response of P. monodon to DIV1 under different conditions. In the experimental set-up, the effect of high water temperature (34±1 °C) compared with room temperature (26±1 °C) was investigated. DIV1 replication was significantly inhibited in the high-temperature group (H), resulting in complete viral elimination within 15 days. DIV1 did not resurface even after return to room temperature (26±1 °C), indicating sustained antiviral effects. Compared with the room temperature (26±1 °C) group (N), the H group showed a 100% reduction in the incidence of latent and acute infection. Exposure to high water temperature directly impaired the viability of DIV1, enhancing the immune system of P. monodon, and expediting metabolic processes for efficient DIV1 clearance. The study highlights the significant inhibitory effects of high water temperature (34±1 °C) on DIV1 infection in P. monodon, resulting in viral eradication. This discovery offers a potential strategy for mitigating DIV1 infections in shrimp aquaculture, prompting further investigation into underlying mechanisms. Optimising parameters and protocols for high-temperature treatment is crucial for viral control. Exploring the broader implications of the findings on other viral infections in crustacean aquaculture could provide valuable insights for comprehensive disease prevention and control.

Raffinose Family Oligosaccharides (RFOs) are a kind of polysaccharide containing D-galactose, and they widely exist in higher plants. Synthesis of RFOs begins with galactinol synthase (GolS; EC 2.4.1.123) to convert myo-inositol into galactinol. The subsequent formation of raffinose and stachyose are catalyzed by raffinose synthase (RS; EC 2.4.1.82) and stachyose synthase (STS; EC 2.4.1.67) using sucrose and galactinol as substrate, respectively. The hydrolysis of RFOs is finished by α-galactosidase (α-Gal; EC 3.2.1.22) to produce sucrose and galactose. Importance of RFOs metabolism have been summarized, e.g. In RFOs translocating plants, the phloem loading and unloading of RFOs are widely reported in mediating the plant development process. Interference function of RFOs synthesis or hydrolysis enzymes caused growth defect. In addition, the metabolism of RFOs involved in the biotic or abiotic stresses was discussed in this review. Overall, this literature summarizes our current understanding of RFOs metabolism and points out knowledge gaps that need to be filled in future.

Autophagy serves as the primary intracellular degradation mechanism in which damaged organelles and self-cytoplasmic proteins are transported to the lysosome for degradation. Crohn's disease, an idiopathic chronic inflammatory disorder of the gastrointestinal tract, manifests in diverse regions of the digestive system. Recent research suggests that autophagy modulation may be a new avenue for treating Crohn's disease, and several promising small-molecule modulators of autophagy have been reported as therapeutic options. In this review, we discuss in detail how mutations in autophagy-related genes function in Crohn's disease and summarize the modulatory effects on autophagy of small-molecule drugs currently used for Crohn's disease treatment. Furthermore, we delve into the therapeutic potential of small-molecule autophagy inducers on Crohn's disease, emphasizing the prospects for development in this field. We aim to highlight the significance of autophagy modulation in Crohn's disease, with the aspiration of contributing to the development of more efficacious treatments that can alleviate their suffering, and improve their quality of life.

Engineering microbial cell factories has been widely used to produce a variety of chemicals, including natural products, biofuels, and bulk chemicals. However, poor robustness limits microbial production on an industrial scale. Microbial robustness is essential to ensure reliable and sustainable production of targeted chemicals. In this study, we developed an approach to screen transcription factors to improve robustness using CRSPRa technology. We applied this approach to identify some transcription factors to increase the robustness of Escherichia coli to aromatic chemicals. Activation of hdfR, yldP, purR, sosS, ygeH, cueR, cra, and treR increased the robustness of E. coli to phenyllactic acid. Upregulation of some transcription factors also improved the robustness to caffeic acid (cra) or tyrosol (cra, cueR, treR, soxS, hdfR and purR). Our study demonstrated that transcription factor engineering using CRISPRa is a powerful method to increase microbial robustness. This research provides new approaches to efficiently find genes responsible for increasing microbial robustness.

In response to the changing intertidal environment, intertidal macroalgae have evolved complicated Ci utilization mechanisms. However, our knowledge regarding the CO₂ concentrating mechanism (CCM) of macroalgae is limited. Carbonic anhydrase (CA), a key component of CCM, plays essential roles in many physiological reactions in various organisms. While many genes encode CA in the Pyropia yezoensis genome, the exact function of specific CA in P. yezoensis remains elusive. To explore the particular function of chloroplast CA in intertidal macroalgae, we produced chloroplast-localized βCA1 knockdown mutants of P. yezoensis through RNA interference, and Pyβca1i mutants (hereinafter referred to as ca1i) showed a notable decrease in leaf area and overall biomass, as well as decreased soluble protein and unsaturated fatty acid content under different DIC conditions. However, ca1i mutants showed relatively higher starch content compared to the wild-type. The activity of enzymes involved in the Calvin cycle, photorespiration, Pentose-phosphate pathway, and floridean starch synthesis of P. yezoensis indicated an effective starch accumulation pathway after the interference of βCA1. All results suggest that the decreased activity of PyβCA1 impaired the CCM and development of thalli of P. yezoensis, but stimulated starch accumulation in the cytoplasm through feedback to the photorespiration pathway and pentose phosphate pathway to replenish intermediates for the Calvin cycle. This study is the first to explore the specific function of chloroplast CA in intertidal macroalgae using genomic technology. The results provide valuable insights into the adaption mechanisms of intertidal macroalgae to their environment.

The global demand for animal-derived foods has led to a substantial expansion in ruminant production, which has raised concerns regarding methane emissions. To address these challenges, microalgal species that are nutritionally-rich and contain bioactive compounds in their biomass have been explored as attractive feed additives for ruminant livestock production. In this review, we discuss the different microalgal species used for this purpose in recent studies, and review the effects of microalgal feed supplements on ruminant growth, performance, health, and product quality, as well as their potential contributions in reducing methane emissions. We also examine the potential complexities of adopting microalgae as feed additives in the ruminant industry.

Somatic clonal expansion refers to the proliferation and expansion of a cell clone within a multicellular organism. Since cancer also results from the uncontrolled proliferation of few cell clones, it is generally believed that aging-associated somatic clonal expansion observed in normal tissues represents a precancerous condition. For instance, hematological malignancy is often preceded by clonal hematopoiesis. However, the precise connection between cancer and somatic clonal expansion remains elusive in solid organs. In this study, we utilized a straightforward method to assess the relative quantitative degrees of clonal expansion in nine human organs. Our findings reveal that the degree of clonal expansion varies across different organs while remaining consistent among different individuals. Contrary to the general belief, we did not identify any significant correlation between lifetime cancer risk and the degree of lifetime somatic clonal expansion. For example, the lifetime risk of colorectal cancer is approximately 20 times higher than that of esophageal cancer, yet the former exhibited the lower degree of clonal expansion than the latter. Our results suggest that somatic clonal expansion represents an evolutionary process distinct from carcinogenesis in normal tissues, providing novel perspectives on precancerous conditions.

Macroautophagy, commonly referred to as autophagy, is an evolutionarily conserved cellular process that plays a crucial role in maintaining cellular homeostasis. It orchestrates the delivery of dysfunctional or surplus cellular materials to the vacuole or lysosome for degradation and recycling, particularly during adverse conditions. Over the past few decades, research has unveiled intricate regulatory mechanisms governing autophagy through various post-translational modifications (PTMs). Among these PTMs, acetylation modification has emerged as a focal point in yeast and animal studies. It plays a pivotal role in autophagy by directly targeting core components within the central machinery of autophagy, including autophagy initiation, nucleation, phagophore expansion, and autophagosome maturation. Additionally, acetylation modulates autophagy at the transcriptional level by modifying histones and transcription factors. Despite its well-established significance in yeast and mammals, the role of acetylation in plant autophagy remains largely unexplored, and the precise regulatory mechanisms remain enigmatic. In this comprehensive review, we summarize the current understanding of the function and underlying mechanisms of acetylation in regulating autophagy across yeast, mammals, and plants. We particularly highlight recent advances in deciphering the impact of acetylation on plant autophagy. These insights not only provide valuable guidance but also inspire further scientific inquiries into the intricate role of acetylation in plant autophagy.

Autosomal dominant polycystic kidney disease (ADPKD) is a dominant genetic disorder caused primarily by mutations in the PKD1 gene, resulting in the formation of numerous cysts and eventually kidney failure. However, there are currently no gene therapy studies aimed at correcting PKD1 gene mutations. In this study, we identified two mutation sites associated with ADPKD, c.1198 (C>T) and c.8311 (G>A), which could potentially be corrected by adenine base editor (ABE). The correction efficiencies of different ABE variants were tested using the HEK293T-PKD1 c.1198 (C>T) and HEK293T-PKD1 c.8311 (G>A) reporter cell lines. We then generated induced pluripotent stem cells (iPSCs^mut/WT) from the peripheral blood mononuclear cells (PBMCs) of the heterozygous patient to develop a disease cell model. Since the iPSCs^mut/WT did not exhibit a typical disease phenotype in stem cell status, differentiation into kidney organoids in vitro led to the expression of kidney organ-specific marker proteins. Stimulation of cAMP signaling with forskolin resulted in cystic expansion of renal epithelial tissue in iPSC^mut/WT-derived kidney organoids, resembling the cystic phenotype observed in ADPKD patients. However, kidney organoids differentiated from ABE-corrected iPSCs did not display the cystic phenotype. Furthermore, we used a dual AAV split-ABEmax system as a therapeutic strategy and achieved an average editing efficiency of approximately 6.56% in kidney organoids. Overall, this study provides a framework for gene therapy targeting ADPKD through ABE single-base editing, offering promising prospects for future therapeutic interventions.