Cold Spring Harbor perspectives in biology最新文献

This paper argues that the historiography of genetics ∼1900, the formation period of modern science, is too narrow. It lacks attention to plant breeding. Perhaps this omission also narrows the present understanding of fundamental ideas like the genotype/phenotype distinction and the gene concept? There is a mythical story still told in textbooks and at anniversaries: As modern genetics started with the rediscovery of Mendel's laws in 1900, a fateful controversy over continuous or discontinuous variation of heredity between biometricians and Mendelians. Discontinuity appeared as a threat to the Darwinian theory of evolution by natural selection. Only by the 1920s was the problem solved by a theory of population genetics founded on the chromosome theory of heredity.¹ However, in plant breeding ∼1900 ideas of heredity and evolution were closely intertwined, and the combination of discontinuous heredity with continuous Darwinian evolution was an obvious option.

Two things about Mendel were "rediscovered" in 1900: His famous paper of 1865 and the story of his life and long neglect. Unlike the paper, which anyone could read in its entirety, the story came out only gradually, and many of its elements were misconstrued by Western European scientists. They pictured him as a pure scientist like themselves and were puzzled by or disinterested in his career as a clergyman, his intellectual community in far-off Moravia, and the importance to him of practical plant breeding. This paper recapitulates the process of mythmaking that followed the rediscovery, then shows how more recent historical research has been able to undo it and, in a sense, "unrediscover" Mendel.

Whereas Mendelian genetics is an important research program in the life sciences, its school version is problematic. On the one hand, it contains stereotypical representations of Gregor Mendel's work that misrepresent his findings and the historical context. This deprives students from gaining an authentic picture of how science is done. On the other hand, what most students end up learning in schools are extremely simplistic accounts of heredity, whereby alleles directly control traits and phenotypes, and thus exclusively depend on which allele an individual has. Such oversimplifications of Mendelian genetics as those that we still teach in schools were exploited by ideologues in the beginning of the twentieth century to provide the presumed "scientific" basis for eugenics. This paper addresses these problems of the school version of Mendelian genetics, which I call "naive" Mendelian genetics. It also proposes a shift in school education from teaching how the science of genetics is done using model systems to teaching the complexities of development through which heredity is materialized.

Skeletal muscle is one of the tissues with the highest range of variability in metabolic rate, which, to a large extent, is critically dependent on tightly controlled and fine-tuned mitochondrial activity. Besides energy production, other mitochondrial processes, including calcium buffering, generation of heat, redox and reactive oxygen species homeostasis, intermediate metabolism, substrate biosynthesis, and anaplerosis, are essential for proper muscle contractility and performance. It is thus not surprising that adequate mitochondrial function is ensured by a plethora of mechanisms, aimed at balancing mitochondrial biogenesis, proteostasis, dynamics, and degradation. The fine-tuning of such maintenance mechanisms ranges from proper folding or degradation of individual proteins to the elimination of whole organelles, and in extremis, apoptosis of cells. In this review, the present knowledge on these processes in the context of skeletal muscle biology is summarized. Moreover, existing gaps in knowledge are highlighted, alluding to potential future studies and therapeutic implications.

Astrocytes are predominant glial cells that tile the central nervous system and participate in well-established functional and morphological interactions with neurons, blood vessels, and other glia. These ubiquitous cells display rich intracellular Ca²⁺ signaling, which has now been studied for over 30 years. In this review, we provide a summary and perspective of recent progress concerning the study of astrocyte intracellular Ca²⁺ signaling as well as discussion of its potential functions. Progress has occurred in the areas of imaging, silencing, activating, and analyzing astrocyte Ca²⁺ signals. These insights have collectively permitted exploration of the relationships of astrocyte Ca²⁺ signals to neural circuit function and behavior in a variety of species. We summarize these aspects along with a framework for mechanistically interpreting behavioral studies to identify directly causal effects. We finish by providing a perspective on new avenues of research concerning astrocyte Ca²⁺ signaling.

How barriers to gene flow arise and are maintained are key questions in evolutionary biology. Speciation research has mainly focused on barriers that occur either before mating or after zygote formation. In comparison, postmating prezygotic (PMPZ) isolation-a barrier that acts after gamete release but before zygote formation-is less frequently investigated but may hold a unique role in generating biodiversity. Here we discuss the distinctive features of PMPZ isolation, including the primary drivers and molecular mechanisms underpinning PMPZ isolation. We then present the first comprehensive survey of PMPZ isolation research, revealing that it is a widespread form of prezygotic isolation across eukaryotes. The survey also exposes obstacles in studying PMPZ isolation, in part attributable to the challenges involved in directly measuring PMPZ isolation and uncovering its causal mechanisms. Finally, we identify outstanding knowledge gaps and provide recommendations for improving future research on PMPZ isolation. This will allow us to better understand the nature of this often-neglected reproductive barrier and its contribution to speciation.

The nervous system comprises a remarkably diverse and complex network of cell types, which must communicate with one another with speed, reliability, and precision. Thus, the developmental patterning and maintenance of these cell populations and their connections with one another pose a rather formidable task. Emerging data implicate microglia, the resident myeloid-derived cells of the central nervous system (CNS), in spatial patterning and synaptic wiring throughout the healthy, developing, and adult CNS. Importantly, new tools to specifically manipulate microglia function have revealed that these cellular functions translate, on a systems level, to effects on overall behavior. In this review, we give a historical perspective of work to identify microglia function in the healthy CNS, and highlight exciting new discoveries about their contributions to CNS development, maintenance, and plasticity.