Trends in Genetics最新文献

The genetic code is nearly universal across life. Yet, The National Center for Biotechnology Information (NCBI) genetic code table recognises 27 distinct variants, most of which are confined to eukaryotic nuclei and organelles. Comparative genomics and synthetic recoding studies reveal that the code is far more flexible than once believed, but why has the standard code remained so remarkably conserved among prokaryotes? Here, we propose that horizontal gene transfer (HGT) acts as a stabilising evolutionary force by enforcing translational compatibility among gene-sharing organisms. In prokaryotes, extensive HGT among prokaryotes creates strong selection for code uniformity, whereas genetic isolation in eukaryotes, driven by sexual reproduction, compartmentalisation, and reduced DNA exchange, has permitted divergence. This dynamic parallels human languages: communities that communicate frequently maintain a shared language, while isolated groups develop distinct ones. Although mobile genetic elements can locally perturb decoding through recoding and translational hijacking, these effects rarely propagate across microbial communities. We argue that the near universality of the genetic code is not a frozen historical accident but an emergent property of dense microbial connectivity shaped by HGT.

Modern biomedical genomics has principally centered on disease, leveraging genomic insights to identify disease-associated genotypes. While valuable, this approach is overly reliant on a positivist, disease-centric perspective that often goes hand-in-hand with patterns like deficit framing, racialized medical stereotyping, and genetic determinism. These practices and their underlying beliefs are detrimental for patients, who experience worse health outcomes as a result, and for participant communities, who endure associated stigmas. This commentary seeks to examine the consequences of this narrow lens and to describe the benefits of an alternative approach: salutogenomics, which highlights the full spectrum of human health. Additionally, we explore how adopting diverse knowledge production paradigms could refashion Western genomic methodologies.

Gene expression noise underlies cell-to-cell variability in RNA and protein levels of a seemingly homogeneous population of cells. Emerging evidence suggests a functional role for this variability in the specification of cell fates during mammalian development. Advances in genome-wide and single-cell technologies now enable the quantification and deciphering of transcriptome variability with increasing precision. In this review, we highlight recent insights into the significance of gene expression noise during early embryogenesis, focusing on RNA variability. We discuss new approaches to further quantify and unravel different sources of gene expression noise and how this yields insights into early mammalian development.

Despite decades of clubroot research, only three resistance (R) genes have been validated. However, many of the 'new' R genes are, in fact, identical to or allelic with these three. In this forum article we advocate for more concerted efforts to reduce redundancies in reporting 'novel' R genes and to focus on establishing a common nomenclature system.

Transposable elements (TEs) - long considered 'junk DNA' - challenge the binary of threat and therapeutic opportunity in cancer. Their reactivation is not a singular event but a convergence of evolutionary legacy, regulatory disruption, and technological insight. This review synthesizes a growing body of work that positions TEs as both catalysts and antagonists of the tumor state. Across regulatory control, viral mimicry, protein-coding potential, and antigen presentation, TEs blur the line between harm and utility. Each example reflects a broader theme: context defines consequence. By tracing historical shifts and technological advances, we argue for an integrated view: one where TEs are not just anomalies, but dynamic agents in the complexity of cancer.

The genome is packaged with nuclear proteins and RNAs into a complex structure known as chromatin. Its dynamic organization influences genome functions and nuclear properties. Since 2009, high-throughput DNA sequencing methods such as Hi-C and ChIA-PET have pioneered genome-wide mapping of chromatin folding architectures and have given rise to the field of three-dimensional (3D) genome biology. Now, after 15 years of development, this field has experienced a remarkable growth and is still expanding rapidly. It is significantly deepening our understanding of how genome organization affects nuclear functions in various biological systems. In this review we focus on the breakthroughs and expansion of sequencing-based technologies in mapping 3D genomic landscapes and envisage the next frontiers in advancing the 3D genome biology.

The brain's complexity arises from diverse cell types varying spatially and temporally. N⁶-methyladenosine (m⁶A), the most abundant mRNA modification, regulates gene expression and cellular function. While bulk sequencing studies have provided foundational insights, they obscure m⁶A heterogeneity across cell types and brain regions. Recent advances in single-cell and spatial m⁶A detection technologies have revolutionized our understanding, enabling the exploration of cell-type-specific and spatial m⁶A landscapes. This review discusses the limitations of bulk approaches and highlights emerging single-cell and spatial technologies. We also provide a forward-looking perspective on how technological improvements can further uncover m⁶A's role in brain complexity, offering new opportunities to develop targeted therapies for cell-type-specific m⁶A-marked RNAs.

Symbiosis is a fundamental characteristic of eukaryotic biology. Arthropods, including insects, often harbor maternally inherited endosymbiotic microbes, some of which have evolved the ability to selectively kill male hosts - a phenomenon known as 'male killing.' The evolutionary history and mechanisms of symbiont-induced male killing have remained poorly understood. However, recent studies have revealed a remarkable diversity of male-killing strategies and their associated causative genes in diverse bacteria and viruses that target different aspects of the host reproductive system. Some insects have evolved various suppressor genes to counteract male-killing actions. This review synthesizes the current knowledge on the evolution and mechanisms underlying microbe-induced male killing and explores their broader implications for the ecology and evolution of eukaryotic life forms.

The DNA mismatch repair (MMR) system is classically viewed as being anti-recombinogenic during meiosis because it mediates heteroduplex rejection to inhibit homeologous recombination, leading to postzygotic isolation between closely related species. In this forum article, conversely, we summarize a very recent study showing that homologous recombination (HR) proteins can antagonize MMR.

Over the past decade, single-cell omics sequencing technologies have revolutionized biological and medical research and deepened our knowledge of cellular heterogeneities in life activities at the genomic, epigenomic, and transcriptomic levels. Concurrently, single-molecule long-read sequencing (SMS) technologies have also made amazingly rapid progress. In recent years, the convergence of these two exciting fields has injected new vitality into the generation of novel insights in genomics (repetitive elements, structural variations), epigenomics (allele-specific epigenetic modifications), and transcriptomics (alternative splicing) at the single-cell level, providing powerful new tools and opening new opportunities for biomedical fields. In this review, we introduce SMS platform-based single-cell genome, epigenome, and transcriptome sequencing technologies - the current situation and future perspectives.