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Summary The regulation of gene expression plays an essential role in both the phenotype and adaptation of plants. Transcriptome sequencing enables simultaneous identification of exonic variants and quantification of gene expression. Here, we sequenced the leaf transcriptomes of 287 rice accessions from around the world and obtained a total of 177 853 high‐quality single nucleotide polymorphisms after filtering. Genome‐wide association study identified 44 354 expression quantitative trait loci (eQTLs), which regulate the expression of 13 201 genes, as well as 17 local eQTL hotspots and 96 distant eQTL hotspots. Furthermore, a transcriptome‐wide association study screened 21 candidate genes for starch content in the flag leaves at the heading stage. HS002 was identified as a significant distant eQTL hotspot with five downstream genes enriched for diterpene antitoxin synthesis. Co‐expression analysis, eQTL analysis, and linkage mapping together demonstrated that bHLH026 acts as a key regulator to activate the expression of downstream genes. The transgenic assay revealed that bHLH026 is an important regulator of diterpenoid antitoxin synthesis and enhances the disease resistance of rice. These findings improve our knowledge of the regulatory mechanisms of gene expression variation and complex regulatory networks of the rice genome and will facilitate genetic improvement of cultivated rice varieties.

In vertebrates, mainly single genes with an allele ratio of 1:1 trigger sex-determination (SD), leading to initial equal sex-ratios. Such genes are designated master-key regulators (MKRs) and are frequently associated with DNA structural variations, such as copy-number variation and null-alleles. Most MKR knowledge comes from fish, especially cichlids, which serve as a genetic model for SD. We list 14 MKRs, of which dmrt1 has been identified in taxonomically distant species such as birds and fish. The identification of MKRs with known involvement in SD, such as amh and fshr, indicates that a common network drives SD. We illustrate a network that affects estrogen/androgen equilibrium, suggesting that structural variation may exert over-expression of the gene and thus form an MKR. However, the reason why certain factors constitute MKRs, whereas others do not is unclear. The limited number of conserved MKRs suggests that their heterologous sequences could be used as targets in future searches for MKRs of additional species. Sex-specific mortality, sex reversal, the role of temperature in SD, and multigenic SD are examined, claiming that these phenomena are often consequences of artificial hybridization. We discuss the essentiality of taxonomic authentication of species to validate purebred origin before MKR searches.

Aging-related cognitive decline is associated with brain structural changes and synaptic loss. However, the molecular mechanisms of cognitive decline during normal aging remain elusive. Using the GTEx transcriptomic data from 13 brain regions, we identified aging-associated molecular alterations and cell-type compositions in males and females. We further constructed gene co-expression networks and identified aging-associated modules and key regulators shared by both sexes or specific to males or females. A few brain regions such as the hippocampus and the hypothalamus show specific vulnerability in males, while the cerebellar hemisphere and the anterior cingulate cortex regions manifest greater vulnerability in females than in males. Immune response genes are positively correlated with age, whereas those involved in neurogenesis are negatively correlated with age. Aging-associated genes identified in the hippocampus and the frontal cortex are significantly enriched for gene signatures implicated in Alzheimer's disease (AD) pathogenesis. In the hippocampus, a male-specific co-expression module is driven by key synaptic signaling regulators including , , and ; while in the cortex, a female-specific module is associated with neuron projection morphogenesis, which is driven by key regulators including , and . In the cerebellar hemisphere, a myelination-associated module shared by males and females is driven by key regulators such as , , , , and , which have been implicated in the development of AD and other neurodegenerative diseases. This integrative network biology study systematically identifies molecular signatures and networks underlying brain regional vulnerability to aging in males and females. The findings pave the way for understanding the molecular mechanisms of gender differences in developing neurodegenerative diseases such as AD.

Common inflammatome gene signatures as well as disease‐specific signatures were identified by analyzing 12 expression profiling data sets derived from 9 different tissues isolated from 11 rodent inflammatory disease models. The inflammatome signature significantly overlaps with known drug targets and co‐expressed gene modules linked to metabolic disorders and cancer. A large proportion of genes in this signature are tightly connected in tissue‐specific Bayesian networks (BNs) built from multiple independent mouse and human cohorts. Both the inflammatome signature and the corresponding consensus BNs are highly enriched for immune response‐related genes supported as causal for adiposity, adipokine, diabetes, aortic lesion, bone, muscle, and cholesterol traits, suggesting the causal nature of the inflammatome for a variety of diseases. Integration of this inflammatome signature with the BNs uncovered 151 key drivers that appeared to be more biologically important than the non‐drivers in terms of their impact on disease phenotypes. The identification of this inflammatome signature, its network architecture, and key drivers not only highlights the shared etiology but also pinpoints potential targets for intervention of various common diseases. A common inflammatome signature, as well as disease‐specific expression patterns, was identified from 11 different rodent inflammatory disease models. Causal regulatory networks and the drivers of the inflammatome signature were uncovered and validated. Synopsis A common inflammatome signature, as well as disease‐specific expression patterns, was identified from 11 different rodent inflammatory disease models. Causal regulatory networks and the drivers of the inflammatome signature were uncovered and validated. Representative inflammatome gene signatures, as well as disease model‐specific gene signatures, were identified from 12 gene expression profiling data sets derived from 9 different tissues isolated from 11 rodent inflammatory disease models. The inflammatome signature is highly enriched for immune response‐related genes, disease causal genes, and drug targets. Regulatory relationships among the inflammatome signature genes were examined in over 70 causal networks derived from a number of large‐scale genetic studies of multiple diseases, and the potential key drivers were uncovered and validated prospectively. Over 70% of the inflammatome signature genes and over 50% of the key driver genes have not been reported in previous studies of common signatures in inflammatory conditions.

Oreochromis niloticus has been used as a reference genome for studies of tilapia sex determination (SD) revealing segregating genetic loci on linkage groups (LGs) 1, 3, and 23. The master key regulator genes (MKR) underlying the SD regions on LGs 3 and 23 have been already found. To identify the MKR in fish that segregate for the LG1 XX/XY SD-system, we applied short variant discovery within the sequence reads of the genomic libraries of the Amherst hybrid stock, Coptodon zillii and Sarotherodon galilaeus, which were aligned to a 3-Mbp-region of the O. aureus genome. We obtained 66,372 variants of which six were concordant with the XX/XY model of SD and were conserved across these species, disclosing the male specific figla-like gene. We further validated this observation in O. mossambicus and in the Chitralada hybrid stock. Genome alignment of the 1252-bp transcript showed that the figla-like gene’s size was 2664 bp, and that its three exons were capable of encoding 99 amino acids including a 45-amino-acid basic helix–loop–helix domain that is typical of the ovary development regulator—factor-in-the-germline-alpha (FIGLA). In Amherst gonads, the figla-like gene was exclusively expressed in testes. Thus, the figla-like genomic presence determines male fate by interrupting the female developmental program. This indicates that the figla-like gene is the long-sought SD MKR on LG1.

Background: Exposure to early life stress significantly increases the risk of psychopathology later in life. However, the impact of early life stress on the gut microbiome and its potential role in mental health outcomes remains insufficiently understood. This narrative review examines the current knowledge on how early life stress and its associated consequences may affect the gut microbiome, with a particular focus on conditions such as anxiety, depression, and post-traumatic stress disorder. Method: A comprehensive literature search was conducted in the PubMed and Web of Science databases between January and February 2025, covering studies published between 2015 and 2025. Results: Early life stress can profoundly impact cognitive function and neurodevelopment, with maternal early-life nutrition playing a significant role in modulating the effects of prenatal and postnatal stress. Early life stress influences the gut microbiome, disrupting its composition and function by altering the synthesis of microbial metabolites, neurotransmitters, and the activation of key metabolic pathways. However, the precise role of the gut microbiome in modulating stress responses during childhood and adolescence has not yet been fully elucidated. Conclusions: Several studies have demonstrated an association between early life stress and the gut microbiome. However, causality has not yet been established due to the numerous intrinsic and extrinsic factors influencing the microbiome-gut–brain axis. In the coming years, research on key microbial regulators, such as short-chain fatty acids, amino acids, and psychobiotics, may represent a promising approach for addressing central nervous system alterations linked to early life stress. Thus, further studies will be necessary to evaluate their potential as therapeutic agents.

Orchids are the flowers of magnetic beauty. Vivid and attractive flowers with magnificent shapes make them the king of the floriculture industry. However, the long-awaited flowering is a drawback to their market success, and therefore, flowering time regulation is the key to studies about orchid flower development. Although there are some rare orchids with a continuous flowering pattern, the molecular regulatory mechanisms are yet to be elucidated to find applicable solutions to other orchid species. Multiple regulatory pathways, such as photoperiod, vernalization, circadian clock, temperature and hormonal pathways are thought to signalize flower timing using a group of floral integrators. This mini review, thus, organizes the current knowledge of floral time regulators to suggest future perspectives on the continuous flowering mechanism that may help to plan functional studies to induce flowering revolution in precious orchid species.

Oreochromis fishes exhibit variability of sex-determination (SD) genes whose characterization contributes to understanding of the sex differentiation network, and to effective tilapia farming, which requires all-male culture. However, O. niloticus (On) amh is the only master-key regulator (MKR) of SD that has been mapped (XY/XX SD-system on LG23). In O. aureus (Oa), LG3 controls a WZ/ZZ SD-system that has recently been delimited to 9.2 Mbp, with an embedded interval rich with female-specific variation, harboring two paics genes and banf2. Developing genetic markers within this interval and using a hybrid Oa stock that demonstrates no recombination repression in LG3, we mapped the critical SD region to 235 Kbp on the orthologous On physical map (p < 1.5 × 10−26). DNA-seq assembly and peak-proportion analysis of variation based on Sanger chromatograms allowed the characterization of copy-number variation (CNV) of banf2. Oa males had three exons capable of encoding 90-amino-acid polypeptides, yet in Oa females, we found an extra copy with an 89-amino-acid polypeptide and three non-conservative amino acid substitutions, designated as banf2w. CNV analysis suggested the existence of two to five copies of banf2 in diploidic Cichlidae. Disrupting the Hardy–Weinberg equilibrium (p < 4.2 × 10−3), banf2w was concordant with female determination in Oa and in three cichlids with LG3 WZ/ZZ SD-systems (O. tanganicae, O. hornorum and Pelmatolapia mariae). Furthermore, exclusive RNA-seq expression in Oa females strengthened the candidacy of banf2w as the long-sought LG3 SD MKR. As banf genes mediate nuclear assembly, chromatin organization, gene expression and gonad development, banf2w may play a fundamental role inducing female nucleus formation that is essential for WZ/ZZ SD.

The recent dominance of Adelphocoris suturalis Jakovlev as the primary cotton field pest in Bt-cotton-cultivated areas has generated significant interest in cotton pest control research. This study addresses the limited understanding of cotton defense mechanisms triggered by A. suturalis feeding. Utilizing LC-QTOF-MS, we analyzed cotton metabolomic changes induced by A. suturalis, and identified 496 differential positive ions (374 upregulated, 122 downregulated) across 11 categories, such as terpenoids, alkaloids, phenylpropanoids, flavonoids, isoflavones, etc. Subsequent iTRAQ-LC-MS/MS analysis of the cotton proteome revealed 1569 differential proteins enriched in 35 metabolic pathways. Integrated metabolome and proteome analysis highlighted significant upregulation of 17 (89%) proteases in the α-linolenic acid (ALA) metabolism pathway, concomitant with a significant increase in 14 (88%) associated metabolites. Conversely, 19 (73%) proteases in the fructose and mannose biosynthesis pathway were downregulated, with 7 (27%) upregulated proteases corresponding to the downregulation of 8 pathway-associated metabolites. Expression analysis of key regulators in the ALA pathway, including allene oxidase synthase (AOS), phospholipase A (PLA), allene oxidative cyclase (AOC), and 12-oxophytodienoate reductase3 (OPR3), demonstrated significant responses to A. suturalis feeding. Finally, this study pioneers the exploration of molecular mechanisms in the plant–insect relationship, thereby offering insights into potential novel control strategies against this cotton pest.

Lung cancer is one of the most invasive cancers affecting over a million of the population. Non-small cell lung cancer (NSCLC) constitutes up to 85% of all lung cancer cases, and therefore, it is essential to identify predictive biomarkers of NSCLC for therapeutic purposes. Here we use a network theoretical approach to investigate the complex behavior of the NSCLC gene-regulatory interactions. We have used eight NSCLC microarray datasets GSE19188, GSE118370, GSE10072, GSE101929, GSE7670, GSE33532, GSE31547, and GSE31210 and meta-analyzed them to find differentially expressed genes (DEGs) and further constructed a protein–protein interaction (PPI) network. We analyzed its topological properties and identified significant modules of the PPI network using cytoscape network analyzer and MCODE plug-in. From the PPI network, top ten genes of each of the six topological properties like closeness centrality, maximal clique centrality (MCC), Maximum Neighborhood Component (MNC), radiality, EPC (Edge Percolated Component) and bottleneck were considered for key regulator identification. We further compared them with top ten hub genes (those with the highest degrees) to find key regulator (KR) genes. We found that two genes, CDK1 and HSP90AA1, were common in the analysis suggesting a significant regulatory role of CDK1 and HSP90AA1 in non-small cell lung cancer. Our study using a network theoretical approach, as a summary, suggests CDK1 and HSP90AA1 as key regulator genes in complex NSCLC network.