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Contractility describes the relative ability of the heart to eject a stroke volume (SV) at a given prevailing afterload (arterial pressure) and preload (end-diastolic volume; EDV). Various measures of contractility are related to the fraction as the SV/EDV or the ejection fraction, and the dynamics of ejection as determined from maximum pressure rise in the ventricles or arteries or from aortic flow velocities determined by echocardiography. At the cellular level, the ultimate determinant of contractility is the relative tension generation and shortening capability of the molecular motors (myosin cross-bridges) of the sarcomeres as determined by the rates and extent of Ca activation, the turnover kinetics of the cross-bridges, and the relative Ca responsiveness of the sarcomeres. Engagement of the regulatory signaling cascades controlling contractility occurs with occupancy and signal transduction by receptors for neurohumors of the autonomic nervous system as well as growth and stress signaling pathways. Contractility is also determined by the prevailing conditions of pH, temperature, and redox state. Short-term control of contractility is fully expressed during exercise. In long-term responses to stresses on the heart, contractility is modified by cellular remodeling and altered signaling that may compensate for a time but which ultimately may fail, leading to disorders.

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Regulation of Vascular Smooth Muscle Function

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Vascular smooth muscle (VSM) constitutes most of the tunica media in blood vessels and plays an important role in the control of vascular tone. Ca2+ is a major regulator of VSM contraction and is strictly regulated by an intricate system of Ca2+ mobilization and Ca2+ homeostatic mechanisms. The interaction of a physiological agonist with its plasma membrane receptor stimulates the hydrolysis of membrane phospholipids and increases the generation of inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). IP3 stimulates Ca2+ release from the intracellular stores in the sarcoplasmic reticulum. Agonists also stimulate Ca2+ influx from the extracellular space via voltage-gated, receptor-operated, and store-operated channels. Ca2+ homeostatic mechanisms tend to decrease the intracellular free Ca2+ concentration ([Ca2+]i) by activating Ca2+ extrusion via the plasmalemmal Ca2+ pump and the Na+/Ca2+ exchanger and the uptake of excess Ca2+ by the sarcoplasmic reticulum and possibly the mitochondria. A threshold increase in [Ca2+]i activates Ca2+-dependent myosin light chain (MLC) phosphorylation, stimulates actinmyosin interaction, and initiates VSM contraction. The agonist-induced maintained increase in DAG also activates specific protein kinase C (PKC) isoforms, which in turn cause phosphorylation of cytoplasmic substrates that increase the contractile myofilaments force sensitivity to Ca2+ and thereby enhance VSM contraction. Agonists could also activate Rho kinase (ROCK), leading to inhibition of MLC phosphatase and further enhancement of the myofilaments force sensitivity to Ca2+. The combined increases in [Ca2+]i, PKC and ROCK activity cause significant vasoconstriction and could also stimulate VSM hypertrophy and hyperplasia. The protracted and progressive activation of these processes could lead to pathological vascular remodeling and vascular disease.

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This presentation describes the unique anatomy and physiology of the vascular beds that serve the eye. The needs for an unobstructed light path from the cornea to the retina and a relatively fixed corneal curvature and distance between refractive structures pose significant challenges for the vasculature to provide nutrients and remove metabolic waste. To meet these needs, the ocular vascular beds are confined to the periphery of the posterior two thirds of the eye and a surrogate circulation provides a continuous flow of aqueous humor to nourish the avascular cornea, lens and vitreous compartment. The production of aqueous humor (and its ease of egress from the eye) also generates the intraocular pressure (IOP), which maintains the shape of the eye. However, the IOP also exerts a compressing force on the ocular blood vessels that is higher than elsewhere in the body. This is particularly true for the intraocular veins, which must have a pressure higher than IOP to remain patent, and so the IOP is the effective venous pressure for the intraocular vascular beds. Consequently, the ocular circulation operates at a lower perfusion pressure gradient than elsewhere in the body and is more at risk for ischemic damage when faced with low arterial pressure, particularly if IOP is elevated. This risk and the specialized tissues of the eye give rise to the fascinating physiology of the ocular circulations.

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The microcirculation is highly responsive to, and a vital participant in, the inflammatory response. All segments of the microvasculature (arterioles, capillaries, and venules) exhibit characteristic phenotypic changes during inflammation that appear to be directed toward enhancing the delivery of inflammatory cells to the injured/infected tissue, isolating the region from healthy tissue and the systemic circulation, and setting the stage for tissue repair and regeneration. The best characterized responses of the microcirculation to inflammation include impaired vasomotor function, reduced capillary perfusion, adhesion of leukocytes and platelets, activation of the coagulation cascade, and enhanced thrombosis, increased vascular permeability, and an increase in the rate of proliferation of blood and lymphatic vessels. A variety of cells that normally circulate in blood (leukocytes, platelets) or reside within the vessel wall (endothelial cells, pericytes) or in the perivascular space (mast cells, macrophages) are activated in response to inflammation. The activation products and chemical mediators released from these cells act through different well-characterized signaling pathways to induce the phenotypic changes in microvessel function that accompany inflammation. Drugs that target a specific microvascular response to inflammation, such as leukocyte-endothelial cell adhesion or angiogenesis, have shown promise in both the preclinical and clinical studies of inflammatory disease. Future research efforts in this area will likely identify new avenues for therapeutic intervention in inflammation.

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In the intestine, a unique immunological system that is different from the systemic immune system exists to provide adaptive immunity in response to luminal bacteria and dietary antigens. There are many lymphoid cell aggregates called gut-associated lymphoid tissue (GALT) including Peyers patches (PPs), which function as important induction sites for the mucosal immune response. M-cells are present in the epithelium of PPs, having a specialized structure for uptake of macromolecules such as bacteria. In addition to GALT, there are abundant lymphoid cells in the intestinal lamina propria, where they mainly play a role as immune effector cells. A strong innate immune system that mainly consists of dendritic cells, macrophages, and T lymphocytes also exists in the intestinal mucosa to assist the barrier function of intestinal epithelial cells.

The intestinal mucosa thus shows a unique morphological structure with many immune cells being present under physiological conditions. This condition is known as "controlled inflammation." These abundant immune cells also have characteristic functions: they are "negatively regulated" and have been educated not to overreact unnecessarily to the intestinal luminal milieu. Main players that control inflammation of the intestinal mucosa include regulatory cytokines and regulatory T cells which induce oral tolerance to intestinal bacteria and food antigens, and the secretory IgA system. The maintenance of unique immunological activity in the intestine is also related to an organized, orchestrated lymphocyte migratory mechanism called the "common mucosal immune system."

These negative regulatory mechanisms of the intestinal immune system are disturbed in certain disease conditions, causing the immunocompetent cells to respond to food components and commensal bacteria by becoming activated and to overproduce inflammatory cytokines and chemokines. These disease conditions include food allergies, such as celiac disease, and the inflammatory bowel diseases, such as ulcerative colitis and Crohns disease, although their exact etiological mechanisms remain to be revealed.

Table of Contents: Introduction / GALT: Its Structure and Formation / Intestinal Epithelial Cells and Their Immune Function / Innate Immunity in the Intestinal Mucosa / Intraepithelial Lymphocytes (IELs) / Lymphoid Cell Trafficking in Intestinal Immunology / Site of Induction of Mucosal Immunity and Antigen Presentation by Dendritic Cells / Production of Secretory IgA (SIgA) / Effector Site of Acquired Immunity and T Helper Cell Subpopulation / Immune Regulatory System and Oral Tolerance / Food Allergy and Celiac Disease / Inflammatory Bowel Diseases / Enteric Infection with Pathogenic Microbes and Mucosal Immunity / References

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From the perspective of blood flow, blood has some unusual properties: it is a suspension of blood cells of which the red blood cells are most numerous and are both deformable (at moderate and high flow rates) and will aggregate under conditions of slow flow. Also, the cellular volume concentration is high (about 40-45%). These features cause blood to have variable viscosity, dependent on flow conditions, and cause both red blood cell sedimentation and syneresis effects under slow flow conditions (which can lead to rheological artifacts). These effects also cause unusual flow phenomena when blood flows in systems of small diameter vessels (especially for diameters of about 500 m or less). These phenomena are seen in non-uniform cell distributions in vessel cross sections, a cell-poor layer of mostly blood plasma at vessels walls, non-proportionate cellular distribution during blood flow through vascular bifurcations, which leads to a very wide distribution of vessel cellular concentrations (from zero to systemic values) in the smaller vessels of the microcirculation, etc. All these phenomena are discussed in this book, as well as the difficulties presented by in vivo microvessels having non-ideal geometries.

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Three distinct types of contractions perform colonic motility functions. Rhythmic phasic contractions (RPCs) cause slow net distal propulsion with extensive mixing/turning over. Infrequently occurring giant migrating contractions (GMCs) produce mass movements. Tonic contractions aid RPCs in their motor function. The spatiotemporal patterns of these contractions differ markedly. The amplitude and distance of propagation of a GMC are several-fold larger than those of an RPC. The enteric neurons and smooth muscle cells are the core regulators of all three types of contractions. The regulation of contractions by these mechanisms is modifiable by extrinsic factors: CNS, autonomic neurons, hormones, inflammatory mediators, and stress mediators. Only the GMCs produce descending inhibition, which accommodates the large bolus being propelled without increasing muscle tone. The strong compression of the colon wall generates afferent signals that are below nociceptive threshold in healthy subjects. However, these signals become nociceptive; if the amplitudes of GMCs increase, afferent nerves become hypersensitive, or descending inhibition is impaired. The GMCs also provide the force for rapid propulsion of feces and descending inhibition to relax the internal anal sphincter during defecation. The dysregulation of GMCs is a major factor in colonic motility disorders: irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), and diverticular disease (DD). Frequent mass movements by GMCs cause diarrhea in diarrhea predominant IBS, IBD, and DD, while a decrease in the frequency of GMCs causes constipation. The GMCs generate the afferent signals for intermittent short-lived episodes of abdominal cramping in these disorders. Epigenetic dysregulation due to adverse events in early life is one of the major factors in generating the symptoms of IBS in adulthood.

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Intestinal Water and Electrolyte Transport in Health and Disease

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The unique architecture and physiology of the mammalian intestine, together with a tightly coordinated regulatory system, allows for the handling and absorption of as much as 9 L of fluid a day with 98% or greater efficiency. Advances in the past 40 years have made inroads into revealing the intricacies and interplay of numerous ion transporters and their modulators that are responsible for intestinal electrolyte and water transport. Studies of two devastating diseases, the virulent infectious disease cholera and the autosomal recessive disease cystic fibrosis, were largely responsible for this information explosion. These advances have been critical in the development of new therapeutic strategies to combat life-threatening diseases of varying etiologies ranging from enteric infections to cystic fibrosis and inflammatory bowel diseases. Yet, the story is far from complete, and progress needs to continue on translating information gained from reductionistic cell and tissue culture models, in vivo models, and ultimately human studies and on improving therapeutic approaches. This book reviews the current status of our knowledge of fluid transport across the intestine, including the complexities of transcellular and paracellular ion transport down the length of the intestine and how aberrations of normal physiological processes lead to disease.

Table of Contents: Overview / Epithelial Cell and Tissue Architecture / Principles of Transepithelial Electrolyte and Water Movement / Intestinal Architecture and Electrolyte Transport / Electrolyte Transporters--Pumps, Carriers, and Channels / Water Transport / Regulation / Intestinal Disorders and Advances Toward Better Treatment of Intestinal Disorders / Conclusion / References

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The secretions of the exocrine pancreas provide for digestion of a meal into components that are then available for processing and absorption by the intestinal epithelium. Without the exocrine pancreas, malabsorption and malnutrition result. This chapter describes the cellular participants responsible for the secretion of digestive enzymes and fluid that in combination provide a pancreatic secretion that accomplishes the digestive functions of the gland. Key cellular participants, the acinar cell and the duct cell, are responsible for digestive enzyme and fluid secretion, respectively, of the exocrine pancreas. This chapter describes the neurohumoral pathways that mediate the pancreatic response to a meal as well as details of the cellular mechanisms that are necessary for the organ responses, including protein synthesis and transport and ion transports, and the regulation of these responses by intracellular signaling systems. Examples of pancreatic diseases resulting from dysfunction in cellular mechanisms provide emphasis of the importance of the normal physiologic mechanisms.

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Regulation of Endothelial Barrier Function

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The vascular endothelium lining the inner surface of blood vessels serves as the first interface for circulating blood components to interact with cells of the vascular wall and surrounding extravascular tissues. In addition to regulating blood delivery and perfusion, a major function of vascular endothelia, especially those in exchange microvessels (capillaries and postcapillary venules), is to provide a semipermeable barrier that controls bloodtissue exchange of fluids, nutrients, and metabolic wastes while preventing pathogens or harmful materials in the circulation from entering into tissues. During host defense against infection or tissue injury, endothelial barrier dysfunction occurs as a consequence as well as cause of inflammatory responses. Plasma leakage disturbs fluid homeostasis and impairs tissue oxygenation, a pathophysiological process contributing to multiple organ dysfunction associated with trauma, infection, metabolic disorder, and other forms of disease. In this book, we provide an updated overview of microvascular endothelial barrier structure and function in health and disease. The discussion is initiated with the basic physiological principles of fluid and solute transport across microvascular endothelium, followed by detailed information on endothelial cellcell and cellmatrix interactions and the experimental techniques that are employed to measure endothelial permeability. Further discussion focuses on the signaling and molecular mechanisms of endothelial barrier responses to various stimulations or drugs, as well as their relevance to several common clinical conditions. Taken together, this book provides a comprehensive analysis of microvascular endothelial cell and molecular pathophysiology. Such information will assist scientists and clinicians in advanced basic and clinical research for improved health care.

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Multiple Functions of the Endothelial Cells -- Focus on Endothelium-Derived Vasoactive Mediators

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The endothelium, a monolayer of endothelial cells, constitutes the inner cellular lining of the blood vessels (arteries, veins and capillaries) and the lymphatic system, and therefore is in direct contact with the blood/lymph and the circulating cells. The endothelium is a major player in the control of blood fluidity, platelet aggregation and vascular tone, a major actor in the regulation of immunology, inflammation and angiogenesis, and an important metabolizing and an endocrine organ. Endothelial cells controls vascular tone, and thereby blood flow, by synthesizing and releasing relaxing and contracting factors such as nitric oxide, metabolites of arachidonic acid via the cyclooxygenases, lipoxygenases and cytochrome P450 pathways, various peptides (endothelin, urotensin, CNP, adrenomedullin, etc.), adenosine, purines, reactive oxygen species and so on. Additionally, endothelial ectoenzymes are required steps in the generation of vasoactive hormones such as angiotensin II. An endothelial dysfunction linked to an imbalance in the synthesis and/or the release of these various endothelial factors may explain the initiation of cardiovascular pathologies (from hypertension to atherosclerosis) or their development and perpetuation.

Table of Contents: Introduction / Multiple Functions of the Endothelial Cells / Calcium Signaling in Vascular Cells and Cell-to-Cell Communications / Endothelium-Dependent Regulation of Vascular Tone / Conclusion / References

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Process Monitoring and Quality by Design for Biotechnology Products

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Traditional pharmaceutical development is an unwieldy process requiring extensive experimentation and long lead times before process scientists can fully understand the effect that process parameters such as pH, temperature, cell viability, or process yield may have on the product acceptability. Implementation of quality by design is a science-based approach that allows the operating ranges and the acceptance criteria to be established based on the impact on product quality attributes. During manufacturing, process monitoring becomes part of a continuous verification effort and statistical control limits can be used to signal potential trends or drifts in the process. Single manufacturing batches that are aberrant are readily identified. The melding of scientific understanding, information systems architecture, instrumentation, software, and personnel training provides a large return on investment by ensuring that the manufacturing process produces a consistent pharmaceutical product that meets acceptable release standards for human use.

Table of Contents: Abbreviations / Introduction / From the Traditional Development Path to Quality by Design / Continuous Process Verification and Process Monitoring / Process Monitoring and Statistical Control Limits / Multivariate Analysis: A Mature State of Statistical Process Monitoring / Conclusion / Bibliography

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The microcirculation of the gastrointestinal tract is under the control of both myogenic and metabolic regulatory systems. The myogenic mechanism contributes to basal vascular tone and the regulation of transmural pressure, while the metabolic mechanism is responsible for maintaining an appropriate balance between O2 demand and O2 delivery. In the postprandial state, hydrolytic products of food digestion elicit a hyperemia, which serves to meet the increased O2 demand of nutrient assimilation. Metabolically linked factors (e.g., tissue pO2, adenosine) are primarily responsible for this functional hyperemia. The fenestrated capillaries of the gastrointestinal mucosa are relatively permeable to small hydrolytic products of food digestion (e.g., glucose), yet restrict the transcapillary movement of larger molecules (e.g., albumin). This allows for the absorption of hydrolytic products of food digestion without compromising the oncotic pressure gradient governing transcapillary fluid movement and edema formation. The gastrointestinal microcirculation is also an important component of the mucosal defense system whose function is to prevent (and rapidly repair) inadvertent epithelial injury by potentially noxious constituents of chyme. Two pathological conditions in which the gastrointestinal circulation plays an important role are ischemia/reperfusion and chronic portal hypertension. Ischemia/reperfusion results in mucosal edema and disruption of the epithelium due, in part, to an inflammatory response (e.g., increase in capillary permeability to macromolecules and neutrophil infiltration). Chronic portal hypertension results in an increase in gastrointestinal blood flow due to an imbalance in vasodilator and vasoconstrictor influences on the microcirculation.

Table of Contents: Introduction / Anatomy / Regulation of Vascular Tone and Oxygenation / Extrinsic Vasoregulation: Neural and Humoral / Postprandial Hyperemia / Transcapillary Solute Exchange / Transcapillary Fluid Exchange / Interaction of Capillary and Interstitial Forces / Gastrointestinal Circulation and Mucosal Defense / Gastrointestinal Circulation and Mucosal Pathology I: Ischemia/Reperfusion / Gastrointestinal Circulation and Mucosal Pathology II: Chronic Portal Hypertension / Summary and Conclusions / References / Author Biography

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Induction and Segregation of the Vertebrate Cranial Placodes

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During evolution the vertebrate head has acquired a number of unique features including specialized paired sense organs and cranial sensory ganglia. These evolutionary novelties arise from discrete thickenings of the head ectoderm known as cranial placodes. They include the adenohypophyseal, olfactory, lens, trigeminal, profundal, otic, epibranchial and lateral line placodes. While distinct in the derivatives and cell types they will form, all cranial placodes originate from a common preplacodal domain surrounding the anterior neural plate. Recent evidence suggests that the induction of this pre-placodal domain and its subsequent subdivision into individual placodes with specific identities is a multi-step process. Here we describe the development of these placodes and their derivatives and summarize recent advances in the characterization of the repertoire of transcription factors underlying their development. We also review recent studies that have started to address the role of several classes of signaling molecules in placode induction and segregation, including Bone Morphogenetic Proteins, Fibroblast Growth Factors and Wnt molecules.

Table of Contents: Introduction / Cranial Placodes and Their Derivatives / Molecular Identity of Cranial Placodes / Induction and Segregation of the Cranial Placodes / Conclusion / Acknowledgments / References / Author Biographies

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Creating Connections in the Developing Brain

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The corpus callosum is the largest fibre tract in the human brain and subserves many of the brains higher-order functions. Disconnection syndromes resulting from surgical ablation, developmental absence (agenesis of the corpus callosum), disease, or injury of the corpus callosum can have profound consequences on cognition. Callosal development involves an intricate series of sequential and concurrent processes, including telencephalic induction, midline tissue patterning, production and specification of callosal neurons. In addition, axon extension and long-range axonal guidance from one hemisphere to the other are required for functional circuit formation in the contralateral hemisphere. Genetic or traumatic disruption to any part of this sequence is pathogenic. Understanding the key processes involved in callosal development is the first step in providing both better neuropsychological outcomes and improved diagnostic and prognostic tools for congenital disconnection syndromes in the future.

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FGF Signalling in Vertebrate Development

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The fibroblast growth factors (FGFs) represent one of the relatively few families of extracellular signalling peptides that have been shown in recent decades to be key regulators of metazoan development. FGFs are required for multiple processes in both protostome and deuterostome groups. Given the wide range of regulatory roles attributed to the FGFs, it is perhaps not surprising that misregulation of this signalling pathway has been implicated in a number of human disease conditions. The focus of the present review is to look at the fundamental components of the FGF pathway and illustrate how this highly conserved regulatory cassette has been deployed to regulate multiple, diverse processes during vertebrate development. This review will explore examples from several vertebrate model organisms and include discussions of the role of FGF signalling in regulating the establishment of the mesoderm, neural patterning, morphogenesis, myogenesis, limb development, and the establishment of rightleft asymmetry.

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Cell Biology and Therapy -- A Visual Approach

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The mysterious disease of cancer, including breast cancer, has plagued mankind since the dawn of recorded history. Regarding the elusive cause of the disease, the "Father of Medicine," Hippocrates of Athens (460377 BC), wrote that, "For instability is characteristic of the humours and so they may be easily altered by nature and by chance." The enigma has persisted until today. In 1971, then President Richard Nixon signed the National Cancer Act and declared a "War on Cancer." He believed the counsel of scientists and physicians that if sufficient resources were committed to the fight, cancer could be virtually eliminated within 5 years. The prophesy failed. Although mortality from a few cancers, most notably leukemias, has been significantly reduced, carcinomas, cancers of the epithelium, which account for 80% of cancer deaths, remain unchanged. While tremendous advances have taken place in our understanding of the molecular and cellular mechanisms operant in cancer, it has proven exceedingly difficult to prevent the occurrence or to halt the progress of the disease. The very best therapy remains early detection while the primary tumor is small and localized to a single site, followed by removal of the offending growth by surgery and/or radiation. The great challenge of finding a cure confronts us yet, and it is effective intervention at the molecular level that offers our best hope. We still must find the "magic bullet."

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The partition of fluid between the vascular and interstitial compartments is regulated by forces (hydrostatic and oncotic) operating across the microvascular walls and the surface areas of permeable structures comprising the endothelial barrier to fluid and solute exchange, as well as within the extracellular matrix and lymphatics. In addition to its role in the regulation of vascular volume, transcapillary fluid filtration also allows for continuous turnover of water bathing tissue cells, providing the medium for diffusional flux of oxygen and nutrients required for cellular metabolism and removal of metabolic byproducts. Transendothelial volume flow has also been shown to influence vascular smooth muscle tone in arterioles, hydraulic conductivity in capillaries, and neutrophil transmigration across postcapillary venules, while the flow of this filtrate through the interstitial spaces functions to modify the activities of parenchymal, resident tissue, and metastasizing tumor cells. Likewise, the flow of lymph, which is driven by capillary filtration, is important for the transport of immune and tumor cells, antigen delivery to lymph nodes, and for return of filtered fluid and extravasated proteins to the blood. Given this background, the aims of this treatise are to summarize our current understanding of the factors involved in the regulation of transcapillary fluid movement, how fluid movements across the endothelial barrier and through the interstitium and lymphatic vessels influence cell function and behavior, and the pathophysiology of edema formation.

Table of Contents: Fluid Movement Across the Endothelial Barrier / The Interstitium / The Lymphatic Vasculature / Pathophysiology of Edema Formation

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Maternal Control of Development in Vertebrates

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Eggs of all animals contain mRNAs and proteins that are supplied to or deposited in the egg as it develops during oogenesis. These maternal gene products regulate all aspects of oocyte development, and an embryo fully relies on these maternal gene products for all aspects of its early development, including fertilization, transitions between meiotic and mitotic cell cycles, and activation of its own genome. Given the diverse processes required to produce a developmentally competent egg and embryo, it is not surprising that maternal gene products are not only essential for normal embryonic development but also for fertility. This review provides an overview of fundamental aspects of oocyte and early embryonic development and the interference and genetic approaches that have provided access to maternally regulated aspects of vertebrate development. Some of the pathways and molecules highlighted in this review, in particular, Bmps, Wnts, small GTPases, cytoskeletal components, and cell cycle regulators, are well known and are essential regulators of multiple aspects of animal development, including oogenesis, early embryogenesis, organogenesis, and reproductive fitness of the adult animal. Specific examples of developmental processes under maternal control and the essential proteins will be explored in each chapter, and where known conserved aspects or divergent roles for these maternal regulators of early vertebrate development will be discussed throughout this review.

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Wnt/?-Catenin Signaling in Vertebrate Posterior Neural Development

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The Wnt/-catenin signaling pathway is a key regulator of cell fate specification, differentiation, and growth in multiple systems throughout the animal kingdom. In vertebrate posterior neural development, Wnt/-catenin signaling controls this complex multistep process. It initially induces the posterior regions of the nervous system, including the mid-hindbrain border, hindbrain, spinal cord and neural crest, and then subsequently fine-tunes the pattern of each region and determines the different cell fates within them. In this review, we explore the function of the Wnt/-catenin pathway during the formation of these specific posterior neural regions. We have examined the important transcriptional targets of the Wnt/-catenin pathway acting downstream to mediate its morphogenetic activity. Different regulatory networks are activated in different posterior neural regions, and these networks induce specific neural cell types in each region. Eludidating how each of these networks specify different cell fates is crucial for understanding the basic tenets of how Wnt morphogenetic activity induces the posterior nervous system during the earliest stages of vertebrate development.