Annual review of cell and developmental biology最新文献

Epigenetic inheritance of repressed chromatin domains plays a central role in the stable silencing of cell type-specific genes and transposons in eukaryotes. Silent chromatin domains are associated with repressive histone modifications, and their propagation requires a read-write mechanism involving recognition of histone modifications by enzymes that also catalyze them. The recycling of parental histones during DNA replication plays a crucial role in maintaining chromatin states by providing the substrate for read-write enzymes. Here we describe recent advances in understanding how the DNA replication machinery and its associated histone chaperones mediate symmetrical parental histone transfer to newly replicated daughter DNA strands and evidence that this process is required for the epigenetic inheritance of silent chromatin domains.

Neurodevelopment is the transformation of genetic information into diverse neuronal phenotypes. Developmental signals initiate patterns of gene transcription and translation that drive progenitors toward a great variety of neurons and nervous systems. The potential from messenger RNA is translated by the ribosome into protein, transforming genetic information into action throughout the cell. This review traces the molecular logic of neurodevelopment to the translation of the proteome and its phenotypes. It highlights emerging research in the neocortex, an evolutionarily recent brain region of complex cognition, where the ribosome is a sensor of developmental signals and translation is a regulator of neuronal fate commitment. Neuronal fates primed in the transcriptome of neural progenitors may be selectively translated, adding layers of spatial and temporal information to the execution of neuronal differentiation. This review aims to advance prior transcription-focused concepts toward their ultimate translation-driven outcomes in the molecular model of neurodevelopment and evolution.

RNAs are versatile polynucleotides that perform essential functions in coding, regulation, catalysis, and structural organization across all forms of life. While most RNAs function endogenously within an organism, certain RNAs, including small RNAs, messenger RNAs, long noncoding RNAs, and other RNA species, can cross organismal boundaries and regulate cellular processes in recipient organisms, a phenomenon termed "cross-kingdom" or "cross-species" RNA communication. These transferred RNAs play a pivotal role in regulating host-microbe interactions. Extracellular vesicles (EVs) are lipid bilayer-enclosed structures that serve as vehicles for transporting RNAs and other cargoes from donor to recipient cells or organisms to regulate diverse cellular processes. This review summarizes recent advances in our understanding of EVs and their functions in shuttling regulatory molecules, especially RNAs, between hosts and microbes, between hosts and parasites or pests, and even between microbes. Elucidating these mechanisms will enable the development of innovative crop protection strategies.

Development depends on the coordinated activity of many genes acting across time and space within each individual, yet many species can produce multiple discrete phenotypes. Such complex balanced polymorphisms are often controlled by supergenes, which are genomic regions containing tightly linked genetic elements that function together to direct alternative developmental programs. Supergene-controlled polymorphisms provide powerful models for understanding evolution and development, revealing how stable alternative fates emerge through the modulation of gene regulatory networks (GRNs). Here, we synthesize recent advances in the evolution, function, and developmental genetics of butterfly mimicry supergenes. We use these historically important systems to review how and why supergenes evolve. We then discuss how supergenes control the development of alternate wing patterns through GRN modification. Finally, we draw parallels with supergene polymorphisms in other organisms to frame general principles governing the evolution and developmental basis of balanced polymorphisms.

A plant's indeterminate growth requires constant cell proliferation and stem cell maintenance to support its developmental plasticity. The root meristem is an excellent system to study the developmental control of plant cell cycles due to the organ's accessibility and the tight link between cell cycle and developmental regulation. Studies have uncovered diverse pathways that shape root tissue patterning and cell identity, but how these mechanistically connect to cell cycle components remains unclear. Recent work and new approaches are starting to bridge this gap. In this review, we synthesize recent findings on the developmental regulation of cell cycle progression across distinct cell types and developmental zones in the Arabidopsis thaliana root apical meristem, highlighting cells and regions of the root where these processes have been thoroughly studied, and others where we know little. These discoveries reveal a nuanced relationship between cell identity and cell cycle regulation that implies an active role for cell cycle modulation in the patterning and developmental plasticity that are integral to plant growth.

Local protein synthesis is a conserved mechanism that allows cells with intricate architectures to perform compartment-specific functions. By translating messenger RNAs (mRNAs) at distinct subcellular locations, cells can respond swiftly and precisely to localized stimuli. This strategy is crucial in neurons, whose long processes extend far from the cell body. Disruptions in neuronal local translation have been implicated in neurological disorders, including fragile X syndrome, amyotrophic lateral sclerosis, and spinal muscular atrophy. While much of the spotlight has been on neurons, glial cells-microglia, astrocytes, oligodendrocytes, and radial glia-are increasingly recognized for their own dynamic use of local translation. These support cells exhibit asymmetric mRNA localization, suggesting that local protein synthesis plays key roles in their diverse functions. This review explores the emerging landscape of local translation in glial cells and examines how this finely tuned process contributes to both normal brain function and the development of neurological disease.

Small proteins, known as microproteins, typically consisting of fewer than 150 amino acids, have recently emerged as a previously unrecognized class of functional proteins in biology. Advances in ribosome profiling, proteogenomics, and genome-wide functional screens have revealed that thousands of small open reading frames are actively translated, producing microproteins, some of which regulate essential processes in metabolism, immunity, cancer, and neurodegeneration. These discoveries have challenged long-held assumptions that gene function is confined to large, conserved proteins and have underscored microproteins as critical modulators. Dysregulation or mutation of small open reading frame-encoding microproteins contributes to a diverse range of biology, and in some cases links the noncanonical proteome to pathophysiological biology. In this review, we summarize current knowledge of microprotein discovery and function, describe key examples connecting microproteins to human disease, and discuss the opportunities and challenges that define this rapidly evolving field.

Transcription is a key process in the life of cells. In the 1990s, cell biologists observed that transcription often takes place in discrete transcription bodies in eukaryotic nuclei, which has sparked an exciting new field of research. Transcription bodies are sites of accumulated transcriptional machinery that regulate the transcription of one or multiple genes. In recent years, we have begun to understand the relationships between transcription bodies and the genome, how transcription bodies assemble, and how they impact transcriptional activity. Much, however, remains unclear: for example, how specificity in the clustering of proteins is achieved, how multiple genes come together in nuclear space, how the dynamic behavior of transcription bodies impacts their function, and in which ways transcription bodies affect transcription. In this review, we provide an overview of the current state of knowledge, as well as the open questions, and how these may be addressed using emerging technologies.

The scaling relationship between metabolic rate and body mass is a foundational principle in biology that links physiology, ecology, and evolution. From early empirical studies-most notably Kleiber's observation of 3/4 power law scaling-to contemporary theoretical frameworks, decades of research have sought to explain why organismal metabolic rate increases more slowly than body mass. This review examines variation in scaling exponents across the tree of life and explores how cellular features, including cell size, mitochondrial dynamics, and energy storage, shape whole-organism metabolism. We describe how dynamic metabolic rates during embryonic development reveal patterns of energy use during growth, while deviations in metabolic scaling across species and disease states indicate how biological systems balance energy constraints with adaptive flexibility. Together, these insights position cells as the critical interface linking molecular bioenergetics to organismal function, evolution, and ecology.

Seventy years of developmental studies have identified the cellular framework and key developmental mechanisms underpinning mammalian kidney development. This understanding has centered on rodent research, where developmental genetics in the mouse has played a particularly important role. Over the last decade, the application of developmental insight to human pluripotent stem cells, generating human cell and organoid models, has spotlighted therapeutic opportunity. This review considers human kidney development and how developmental insight is being applied toward the generation of functional human kidney cell types in pluripotent stem cell-derived kidney models and provides a perspective on advancing models for clinical impact.