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- Volume 25, 2009
Annual Review of Cell and Developmental Biology - Volume 25, 2009
Volume 25, 2009
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From Mouse Egg to Mouse Embryo: Polarities, Axes, and Tissues
Vol. 25 (2009), pp. 483–512More LessThis review describes the three classical models (mosaic, positional, and polarization) proposed to explain blastocyst formation and summarizes the evidence concerning them. It concludes that the polarization model incorporates elements of the other two models and best explains most known information. I discuss key requirements of a molecular basis for the generation and stabilization of polarity and identify ezrin/E-cadherin, PAR proteins, and Cdx2 as plausible key molecular players. I also discuss the idea of a network process operating to build cell allocations progressively into committed differences. Finally, this review critically considers the possibility of developmental information being encoded within the oocyte and zygote. No final decision can be reached on a mechanism of action underlying any encoded information, but a cell interaction process model is preferred over one that relies solely on differential inheritance.
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Conflicting Views on the Membrane Fusion Machinery and the Fusion Pore
Vol. 25 (2009), pp. 513–537More LessFast exocytosis of synaptic vesicles differs from other membrane fusion reactions by being under tight temporal control by the intracellular calcium concentration. This is achieved by subjecting the SNARE-dependent fusion pathway to additional layers of control, both upstream and downstream of the assembly of the fusogenic SNARE-complex. Here, I review conflicting views on the function of the core fusion machinery consisting of the SNAREs, Munc18, complexin, and synaptotagmin. Munc18 controls docking of vesicles to the plasma membrane and initial SNARE-complex assembly, whereas complexin and synaptotagmin cooperate in holding the SNARE complex in an intermediate release-ready or cocked state. Different effects of complexin and synaptotagmin shape the energy landscape for fusion and make final fusion calcium triggered. The final steps are fusion pore formation and expansion, which allow release of the water-soluble vesicle content. The fusion pore remains the most elusive part of the exocytosis pathway, owing to its short lifetime.
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Coordination of Lipid Metabolism in Membrane Biogenesis
Vol. 25 (2009), pp. 539–566More LessBilayer synthesis during membrane biogenesis involves the concerted assembly of multiple lipid species, requiring coordination of the level of lipid synthesis, uptake, turnover, and subcellular distribution. In this review, we discuss some of the salient conclusions regarding the coordination of lipid synthesis that have emerged from work in mammalian and yeast cells. The principal instruments of global control are a small number of transcription factors that target a wide range of genes encoding enzymes that operate in a given metabolic pathway. Critical in mammalian cells are sterol regulatory element binding proteins (SREBPs) that stimulate expression of genes for the uptake and synthesis of cholesterol and fatty acids. From work with Saccharomyces cerevisiae, much has been learned about glycerophospholipid and ergosterol regulation through Ino2p/Ino4p and Upc2p transcription factors, respectively. Lipid supply is fine-tuned through a multitude of negative feedback circuits initiated by both end products and intermediates of lipid synthesis pathways. Moreover, there is evidence that the diversity of membrane lipids is maintained through cross-regulatory effects, whereby classes of lipids activate the activity of enzymes operating in another metabolic branch.
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Navigating ECM Barriers at the Invasive Front: The Cancer Cell–Stroma Interface
Vol. 25 (2009), pp. 567–595More LessA seminal event in cancer progression is the ability of the neoplastic cell to mobilize the necessary machinery to breach surrounding extracellular matrix barriers while orchestrating a host stromal response that ultimately supports tissue-invasive and metastatic processes. With over 500 proteolytic enzymes identified in the human genome, interconnecting webs of protease-dependent and protease-independent processes have been postulated to drive the cancer cell invasion program via schemes of daunting complexity. Increasingly, however, a body of evidence has begun to emerge that supports a unifying model wherein a small group of membrane-tethered enzymes, termed the membrane-type matrix metalloproteinases (MT-MMPs), plays a dominant role in regulating cancer cell, as well as stromal cell, traffic through the extracellular matrix barriers assembled by host tissues in vivo. Understanding the mechanisms that underlie the regulation and function of these metalloenzymes as host cell populations traverse the dynamic extracellular matrix assembled during neoplastic states should provide new and testable theories regarding cancer invasion and metastasis.
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The Molecular Basis of Organ Formation: Insights From the C. elegans Foregut
Vol. 25 (2009), pp. 597–628More LessThe digestive tracts of many animals are epithelial tubes with specialized compartments to break down food, remove wastes, combat infection, and signal nutrient availability. C. elegans possesses a linear, epithelial gut tube with foregut, midgut, and hindgut sections. The simple anatomy belies the developmental complexity that is involved in forming the gut from a pool of heterogeneous precursor cells. Here, I focus on the processes that specify cell fates and control morphogenesis within the embryonic foregut (pharynx) and the developmental roles of the pharynx after birth. Maternally donated factors in the pregastrula embryo converge on pha-4, a FoxA transcription factor that specifies organ identity for pharyngeal precursors. Positive feedback loops between PHA-4 and other transcription factors ensure commitment to pharyngeal fate. Binding-site affinity of PHA-4 for its target promoters contributes to the progression of the pharyngeal precursors towards differentiation. During morphogenesis, the pharyngeal precursors form an epithelial tube in a process that is independent of cadherins, catenins, and integrins but requires the kinesin zen-4/MKLP1. After birth, the pharynx and/or pha-4 are involved in repelling pathogens and controlling aging.
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Genetic Control of Bone Formation
Vol. 25 (2009), pp. 629–648More LessIn the past few years, our molecular understanding of bone formation has continued to increase. This review aims to present a comprehensive view of the current state of knowledge in the field. Thus, it will cover our current knowledge of chondrogenesis and osteoblastogenesis. It will also cover the most salient aspects of osteoblast function.
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Listeria monocytogenes Membrane Trafficking and Lifestyle: The Exception or the Rule?
Vol. 25 (2009), pp. 649–670More LessListeria monocytogenes is an intracellular bacterial pathogen that promotes its internalization within nonprofessional phagocytes by interacting with specific host cell receptors. L. monocytogenes resides transiently in a membrane-bound compartment before escaping into the host cell cytosol where bacterial proliferation takes place. Actin-based motility then promotes cell-to-cell pathogen spread. Extensive studies on cytoskeleton rearrangements, membrane trafficking, and other events have established this microorganism as an archetype of cellular function subversion for intracellular parasitism. Here we discuss the most significant membrane trafficking pathways hijacked by L. monocytogenes during the host cell infection process and compare them to those of other intracellular pathogens, in particular Shigella flexneri, Salmonella enterica, and Mycobacterium tuberculosis.
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Asymmetric Cell Divisions and Asymmetric Cell Fates
Vol. 25 (2009), pp. 671–699More LessThe regulation of self-renewal, cell diversity, and differentiation can occur by modulating symmetric and asymmetric cell divisions. Remarkably, asymmetric cell divisions can arise through multiple processes in which molecules in the cytoplasm and nucleus, as well as template “immortal” DNA strands, can segregate to one daughter cell during cell division. Explaining how these events direct distinct daughter cell fates is a major challenge to understanding how the organism is assembled and maintained for a lifetime. Numerous technical issues that are associated with assessing how distinct cell fates are executed in vivo have resulted in divergent interpretations of experimental findings. This review addresses some of these points and considers different developmental model systems that attempt to investigate how cell fate decisions are determined, as well as the molecules that guide these choices.
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Previous Volumes
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Volume 40 (2024)
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Volume 39 (2023)
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Volume 38 (2022)
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Volume 37 (2021)
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Volume 36 (2020)
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Volume 35 (2019)
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Volume 34 (2018)
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Volume 33 (2017)
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Volume 32 (2016)
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Volume 31 (2015)
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Volume 30 (2014)
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Volume 29 (2013)
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Volume 28 (2012)
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Volume 27 (2011)
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Volume 26 (2010)
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Volume 25 (2009)
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Volume 24 (2008)
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Volume 23 (2007)
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Volume 22 (2006)
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Volume 21 (2005)
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Volume 20 (2004)
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Volume 19 (2003)
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Volume 18 (2002)
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Volume 17 (2001)
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Volume 16 (2000)
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Volume 15 (1999)
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Volume 14 (1998)
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Volume 13 (1997)
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Volume 12 (1996)
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Volume 11 (1995)
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Volume 10 (1994)
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Volume 9 (1993)
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Volume 8 (1992)
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Volume 7 (1991)
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Volume 6 (1990)
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Volume 5 (1989)
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Volume 4 (1988)
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Volume 3 (1987)
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Volume 2 (1986)
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Volume 1 (1985)
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Volume 0 (1932)