Annual review of genetics最新文献

Life activities are supported by the intricate metabolic network that is fueled by nutrients. Nutritional and genetic studies in model organisms have determined that dietary restriction and certain mutations in the insulin signaling pathway lead to lifespan extension. Subsequently, the detailed mechanisms of aging as well as various nutrient signaling pathways and their relationships have been investigated in a wide range of organisms, from yeast to mammals. This review summarizes the roles of nutritional and metabolic signaling in aging and lifespan with a focus on amino acids, the building blocks of organisms. We discuss how lifespan is affected by the sensing, transduction, and metabolism of specific amino acids and consider the influences of life stage, sex, and genetic background on the nutritional control of aging. Our goal is to enhance our understanding of how nutrients affect aging and thus contribute to the biology of aging and lifespan.

Neural stem cells (NSCs) are progenitor cell populations generating glial cells and neurons and endowed with long-lasting self-renewal and differentiation potential. While some neural progenitors (NPs) in the embryonic nervous system are also long-lived and match this definition, the term NSC classically refers to such progenitor types in the adult. With the discovery of extensive NSC populations in the adult brain of Danio rerio (zebrafish) and of their high neurogenic activity, including for neuronal regeneration, this model organism has become a powerful tool to characterize and mechanistically dissect NSC properties. On these bases, this article will consider NSCs in the adult zebrafish brain, with a focus on its most extensively characterized domain, the telencephalon (notably its dorsal part, the pallium). Whenever necessary, we will also refer to other brain subdivisions, embryonic processes, and the mouse adult brain, whether for comparative purposes or because more information is available in these other systems.

Polyploidy is a cellular state containing more than two complete chromosome sets. It has largely been studied as a discrete phenomenon in either organismal, tissue, or disease contexts. Increasingly, however, investigation of polyploidy across disciplines is coalescing around common principles. For example, the recent Polyploidy Across the Tree of Life meeting considered the contribution of polyploidy both in organismal evolution over millions of years and in tumorigenesis across much shorter timescales. Here, we build on this newfound integration with a unified discussion of polyploidy in organisms, cells, and disease. We highlight how common polyploidy is at multiple biological scales, thus eliminating the outdated mindset of its specialization. Additionally, we discuss rules that are likely common to all instances of polyploidy. With increasing appreciation that polyploidy is pervasive in nature and displays fascinating commonalities across diverse contexts, inquiry related to this important topic is rapidly becoming unified.

Plants are exposed to temperature conditions that fluctuate over different time scales, including those inherent to global warming. In the face of these variations, plants sense temperature to adjust their functions and minimize the negative consequences. Transcriptome responses underlie changes in growth, development, and biochemistry (thermomorphogenesis and acclimation to extreme temperatures). We are only beginning to understand temperature sensation by plants. Multiple thermosensors convey complementary temperature information to a given signaling network to control gene expression. Temperature-induced changes in protein or transcript structure and/or in the dynamics of biomolecular condensates are the core sensing mechanisms of known thermosensors, but temperature impinges on their activities via additional indirect pathways. The diversity of plant responses to temperature anticipates that many new thermosensors and eventually novel sensing mechanisms will be uncovered soon.

Microbial pathogens have coevolved with their hosts, often for millions of years, and in the process have developed a variety of virulence mechanisms to ensure their survival, typically at the host's expense. At the center of this host-pathogen warfare are proteins called effectors that are delivered by bacteria into their host where they alter the intracellular environment to promote bacterial proliferation. Many effectors are believed to have been acquired by the bacteria from their host during evolution, explaining why researchers are keen to understand their function, as this information may provide insight into both microbial virulence strategies and biological processes that happen within our own cells. Help for accomplishing this goal has come from the recent development of increasingly powerful genetic approaches, which are the focus of this review.

Although the majority of annotated new genes in a given genome appear to have arisen from duplication-related mechanisms, recent studies have shown that genes can also originate de novo from ancestrally nongenic sequences. Investigating de novo-originated genes offers rich opportunities to understand the origin and functions of new genes, their regulatory mechanisms, and the associated evolutionary processes. Such studies have uncovered unexpected and intriguing facets of gene origination, offering novel perspectives on the complexity of the genome and gene evolution. In this review, we provide an overview of the research progress in this field, highlight recent advancements, identify key technical and conceptual challenges, and underscore critical questions that remain to be addressed.

The evolution of the placenta was transformative. It changed how offspring are fed during gestation from depositing all the resources into an egg to continually supplying resources throughout gestation. Placental evolution is infinitely complex, with many moving parts, but at the core it is driven by a conflict over resources between the mother and the baby, which sets up a Red Queen race, fueling rapid diversification of morphological, cellular, and genetic forms. Placentas from even closely related species are highly divergent in form and function, and many cellular processes are distinct. If we could extract the entirety of genomic information for placentas across all species, including the many hundreds that have evolved in fish and reptiles, we could find their shared commonality, and that would tell us which of the many pieces really matter. We do not have this information, but we do have clues. Convergent evolution mechanisms were repeatedly used in the placenta, including the intense selective pressure to co-opt an envelope protein to build a multinucleated syncytium, the use of the same hormones and structural proteins in placentas derived from separate embryonic origins that arose hundreds of millions of years apart, and the co-option of endogenous retroviruses to form capsids as a way of transport and as mutagens to form new enhancers. As a result, the placental genome is the Wild West of biology, set up to rapidly change, adapt, and innovate. This ability to adapt facilitated the evolution of big babies with big brains and will continue to support offspring and their mothers in our ever-changing global environment.

Cold is an important environmental factor limiting plant growth and development. Recent studies have revealed the complex regulatory networks associated with plant responses to cold and identified their interconnections with signaling pathways related to light, the circadian clock, plant hormones, and pathogen defense. In this article, we review recent advances in understanding the molecular basis of cold perception and signal transduction pathways. We also summarize recent developments in the study of cold-responsive growth and flowering. Finally, we propose future directions for the study of long-term cold sensing, RNA secondary structures in response to cold, and the development of cold-tolerant and high-yield crops.

Uncovering the fundamental processes that shape genomic variation in natural populations is a primary objective of population genetics. These processes include demographic effects such as past changes in effective population size or gene flow between structured populations. Furthermore, genomic variation is affected by selection on nonneutral genetic variants, for example, through the adaptation of beneficial alleles or balancing selection that maintains genetic variation. In this article, we discuss the characterization of these processes using population genetic models, and we review methods developed on the basis of these models to unravel the underlying processes from modern population genomic data sets. We briefly discuss the conditions in which these approaches can be used to infer demography or identify specific nonneutral genetic variants and cases in which caution is warranted. Moreover, we summarize the challenges of jointly inferring demography and selective processes that affect neutral variation genome-wide.

The evolution of eusociality in Hymenoptera-encompassing bees, ants, and wasps-is characterized by multiple gains and losses of social living, making this group a prime model to understand the mechanisms that underlie social behavior and social complexity. Our review synthesizes insights into the evolutionary history and molecular basis of eusociality. We examine new evidence for key evolutionary hypotheses and molecular pathways that regulate social behaviors, highlighting convergent evolution on a shared molecular toolkit that includes the insulin/insulin-like growth factor signaling (IIS) and target of rapamycin (TOR) pathways, juvenile hormone and ecdysteroid signaling, and epigenetic regulation. We emphasize how the crosstalk among these nutrient-sensing and endocrine signaling pathways enables social insects to integrate external environmental stimuli, including social cues, with internal physiology and behavior. We argue that examining these pathways as an integrated regulatory circuit and exploring how the regulatory architecture of this circuit evolves alongside eusociality can open the door to understanding the origin of the complex life histories and behaviors of this group.