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Evolution, the logic of biology
By focusing on the cellular mechanisms that underlie ontogeny, phylogeny and regeneration of complex physiologic traits, Evolution, the Logic of Biology demonstrates the use of homeostasis, the fundamental principle of physiology and medicine, as the unifying mechanism for evolution as all of biology. The homeostasis principle can be used to understand how environmental stressors have affected physiologic mechanisms to generate condition-specific novelty through cellular mechanisms.
Evolution, the Logic of Biology allows the reader to understand the vertebrate life-cycle as an intergenerational continuum in support of effective, on-going environmental adaptation. By understanding the principles of physiology from their fundamental unicellular origins, culminating in modern-day metazoans, the reader as student, researcher or practitioner will be encouraged to think in terms of the prevention of disease, rather than in the treatment of disease as the eradication of symptoms. By tracing the ontogeny and phylogeny of this and other phenotypic homologies, one can perceive and understand how complex physiologic traits have mechanistically evolved from their simpler ancestral and developmental origins as cellular structures and functions, providing a logic of biology for the first time.
Evolution, the Logic of Biology will be an invaluable resource for graduate students and researchers studying evolutionary development, medicine and biology, anthropology, comparative and developmental biology, genetics and genomics, and physiology.
eBook
Adaptive oncogenesis : a new understanding of how cancer evolves inside us
\"Popular understanding holds that genetic changes create cancer. James DeGregori uses evolutionary principles to propose a new way of thinking about cancer's occurrence. Cancer is as much a disease of evolution as it is of mutation, one in which mutated cells outcompete healthy cells in the ecosystem of the body's tissues. His theory ties cancer's progression, or lack thereof, to evolved strategies to maximize reproductive success. Through natural selection, humans evolved genetic programs to maintain bodily health for as long as necessary to increase the odds of passing on our genes--but not much longer. These mechanisms engender a tissue environment that favors normal stem cells over precancerous ones. Healthy tissues thwart cancer cells' ability to outcompete their precancerous rivals. But as our tissues age or accumulate damage from exposures such as smoking, normal stem cells find themselves less optimized to their ecosystem. Cancer-causing mutations can now help cells adapt to these altered tissue environments, and thus outcompete normal cells. Just as changes in a species' habitat favor the evolution of new species, changes in tissue environments favor the growth of cancerous cells. DeGregori's perspective goes far in explaining who gets cancer, when it appears, and why. While we cannot avoid mutations, it may be possible to sustain our tissues' natural and effective system of defense, even in the face of aging or harmful exposures. For those interested in learning how cancers arise within the human body, the insights in Cancer: Evolution Within Us offer a compelling perspective\"-- Provided by publisher.
Book
Mouth opening is mediated by separation of dorsal and ventral daughter cells of the lip precursor cells in the larvacean, Oikopleura dioica
Mouth formation involves the processes of mouth opening, formation of the oral cavity, and the development of associated sensory organs. In deuterostomes, the surface ectoderm and the anterior part of the archenteron are reconfigured and reconnected to make a mouth opening. This study of the larval development of the larvacean, Oikopleura dioica, investigates the cellular organization of the oral region, the developmental processes of the mouth, and the formation of associated sensory cells. O. dioica is a simple chordate whose larvae are transparent and have a small number of constituent cells. It completes organ morphogenesis in 7 h, between hatching 3 h after fertilization and the juvenile stage at 10 h, when it attains adult form and starts to feed. It has two types of mechanosensory cell embedded in the oral epithelium, which is a single layer of cells. There are twenty coronal sensory cells in the circumoral nerve ring and two dorsal sensory organ cells. Two bilateral lip precursor cells (LPCs), facing the anterior surface, divide dorsoventrally and make a wedge-shaped cleft between the two daughter cells named the dorsal lip cell (DLC) and the ventral lip cell (VLC). Eventually, the DLC and VLC become detached and separated into dorsal and ventral lips, triggering mouth opening. This is an intriguing example of cell division itself contributing to morphogenesis. The boundary between the ectoderm and endoderm is present between the lip cells and coronal sensory cells. All oral sensory cells, including dorsal sensory organ cells, were of endodermal origin and were not derived from the ectodermal placode. These observations on mouth formation provide a cellular basis for further studies at a molecular level, in this simple chordate.
Journal Article
In search of cell history : the evolution of life's building blocks
The origin of cells remains one of the most fundamental problems in biology, one that over the past two decades has spawned a large body of research and debate. With In Search of Cell History, Franklin M. Harold offers a comprehensive, impartial take on that research and the controversies that keep the field in turmoil.
Written in accessible language and complemented by a glossary for easy reference, this book investigates the full scope of cellular history. Assuming only a basic knowledge of cell biology, Harold examines such pivotal subjects as the relationship between cells and genes; the central role of bioenergetics in the origin of life; the status of the universal tree of life with its three stems and viral outliers; and the controversies surrounding the last universal common ancestor. He also delves deeply into the evolution of cellular organization, the origin of complex cells, and the incorporation of symbiotic organelles, and considers the fossil evidence for the earliest life on earth. In Search of Cell History shows us just how far we have come in understanding cell evolution—and the evolution of life in general—and how far we still have to go.
eBook
POU4F3 pioneer activity enables ATOH1 to drive diverse mechanoreceptor differentiation through a feed-forward epigenetic mechanism
During embryonic development, hierarchical cascades of transcription factors interact with lineage-specific chromatin structures to control the sequential steps in the differentiation of specialized cell types. While examples of transcription factor cascades have been well documented, the mechanisms underlying developmental changes in accessibility of cell type–specific enhancers remain poorly understood. Here, we show that the transcriptional “master regulator” ATOH1—which is necessary for the differentiation of two distinct mechanoreceptor cell types, hair cells in the inner ear and Merkel cells of the epidermis—is unable to access much of its target enhancer network in the progenitor populations of either cell type when it first appears, imposing a block to further differentiation. This block is overcome by a feed-forward mechanism in which ATOH1 first stimulates expression of POU4F3, which subsequently acts as a pioneer factor to provide access to closed ATOH1 enhancers, allowing hair cell and Merkel cell differentiation to proceed. Our analysis also indicates the presence of both shared and divergent ATOH1/POU4F3-dependent enhancer networks in hair cells and Merkel cells. These cells share a deep developmental lineage relationship, deriving from their common epidermal origin, and suggesting that this feed-forward mechanism preceded the evolutionary divergence of these very different mechanoreceptive cell types.
Journal Article
We go way back
\"What is life? How did it start? Long, long ago, no one knows exactly where or when, a tiny bubble formed that was a Little Bit Different. It was the first living cell. Everyone's ancestor. And so the story of life begins.\"-- Front jacket flap.
Book
Clinical characterization and immunosuppressive regulation of CD161 (KLRB1) in glioma through 916 samples
Background Glioblastoma is a paradigm of cancer‐associated immunosuppression, limiting the effects of immunotherapeutic strategies. Thus, identifying the molecular mechanisms underlying immune surveillance evasion is critical. Recently, the preferential expression of inhibitory natural killer (NK) cell receptor CD161 on glioma‐infiltrating cytotoxic T cells was identified. Focusing on the molecularly annotated, large‐scale clinical samples from different ethnic origins, the data presented here provide evidence of this immune modulator's essential roles in brain tumor biology. Methods Retrospective RNA‐seq data analysis was conducted in a cohort of 313 patients with glioma in the Chinese Glioma Genome Atlas (CGGA) database and 603 patients in The Cancer Genome Atlas (TCGA) database. In addition, single‐cell sequencing data from seven surgical specimens of glioblastoma patients and a model in which patient‐derived glioma stem cells were cocultured with peripheral lymphocytes, were used to analyze the molecular evolution process during gliomagenesis. Results CD161 was enriched in high‐grade gliomas and isocitrate dehydrogenase (IDH)‐wildtype glioma. CD161 acted as a potential biomarker for the mesenchymal subtype of glioma and an independent prognostic factor for the overall survival (OS) of patients with glioma. In addition, CD161 played an essential role in inhibiting the cytotoxicity of T cells in glioma patients. During the process of gliomagenesis, the expression of CD161 on different lymphocytes dynamically evolved. Conclusion The expression of CD161 was closely related to the pathology and molecular pathology of glioma. Meanwhile, CD161 promoted the progression and evolution of gliomas through its unique effect on T cell dysfunction. Thus, CD161 is a promising novel target for immunotherapeutic strategies in glioma treatment. CD161 (KLRB1) is a clinical diagnostic marker predicting negative course of patients with gliomas. It plays prominent immune‐evading roles in glioma, and the expression of CD161 on CD8+ lymphocytes gradually increases during glioblastoma genesis.
Journal Article