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[
Nature Reviews Genetics,
2004]
MicroRNAs are a family of small, non-coding RNAs that regulate gene expression in a sequence-specific manner. The two founding members of the microRNA family were originally identified in Caenorhabditis elegans as genes that were required for the timed regulation of developmental events. Since then, hundreds of microRNAs have been identified in almost all metazoan genomes, including worms, flies, plants and mammals. MicroRNAs have diverse expression patterns and might regulate various developmental and physiological processes. Their discovery adds a new dimension to our understanding of complex gene regulatory networks.
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[
The New York Times,
1997]
His tall figure bent over a computer screen in his laboratory at the Massachusetts General Hospital, Dr. Gary Ruvkun rummages through a distant genetic data base for matches to a gene he believes is involved in diabetes. ?You learn how to read these as they are ratcheting by,? he says, while lines of data streak up his screen. ?I think MTV is good training.?
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[
Autophagy,
2024]
Professor Richard (Rick) Morimoto is the Bill and Gayle Cook Professor of Biology and Director of the Rice Institute for Biomedical Research at Northwestern University. He has made foundational contributions to our understanding of how cells respond to various stresses, and the role played in those responses by chaperones. Working across a variety of experimental models, from <i>C</i>. <i>elegans</i> to human neuronal cells, he has identified a number of important molecular components that sense and respond to stress, and he has dissected how stress alters cellular and organismal physiology. Together with colleagues, Professor Morimoto has coined the term "proteostasis" to signify the homeostatic control of protein expression and function, and in recent years he has been one of the leaders of a consortium trying to understand proteostasis in healthy and disease states. I took the opportunity to talk with Professor Morimoto about proteostasis in general, the aims of the consortium, and how autophagy is playing an important role in their research effort.
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[
Journal of Helminthology,
1955]
Osche (1952) has recently published a sorely needed, comprehensive revision of the genus Rhabditis Dujardin [1844] (sensu lato) including detailed study of certain features of the cephalic end, especially of the stoma or mouth cavity. For some time to come his study will surely be the point of departure for morpholigical and systematic work on the group. On the basis principally of the structure of the metastom (a subdivision of the stoma) and of the esophagus, he recognizes some eight subgenera in the genus Rhabditis, which are as follows: Rhabditis Dujardin [1844] (sensu stricto), Choriorhabditis Osche, 1952, Telorhabditis Osche, 1952, Caenorhabditis Osche, 1952, Mesorhabditis Osche, 1952, Teratorhabditis Oshce, 1952, Protorhabditis Osche, 1952, and Parasitorhabditis Fuch, 1937. For all of these save the last he lists the species recognized by him. For a revision of Parasitorhabditis he refers to an unpublished manuscript by Ruhm.....
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[
Trends in Ecology & Evolution,
1999]
In a recent TREE news & comment, Gadagkar made some useful comments on LaMunyon and Ward's interesting study on sexual reproduction in nematodes. I think, however, that he - and LaMunyon and Ward - have confused the benefits of sex for species or demes with those for individuals or genes.
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Connell M, Anderson K, Ainscough R, Blair D, Durbin RM, Dear S, Berks M, Craxton M, Waterston RH, Du Z, Cooper JA, Coulson AR
[
Cold Spring Harb Symp Quant Biol,
1993]
he C. elegans genome project is part of a larger effort to understand how the information encoded in its DNA specifies the biology of this small nematode worm...In this paper we review the construction of the physical map and present a preliminary report on the pilot sequencing project. A more detailed report will be published shortly.
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[
Cell Death and Differentiation,
2004]
The award of the 2002 Nobel Prize to Brenner, Sulston, and Horvitz was one of the most satisfying I can recall, recognizing as it did the long sought meaningful conjunction of developmental biology with cancer research. Cancer is the ultimate derangement of growth and differentiation, affecting as it does the placenta, the embryo, the fetus, the infant, the child, the adolescent, and the adult of any age. Little wonder then that developmental biologists (embryologists in bygone days) have contributed so much to our understanding of cancer's origin. Indeed, the first coherent view of cancer was painted by the great embryologist Theodor Boveri in his heuristic volume of 1914 on the origin of cancer. Having observed the developmental aberrations of sea urchin embryos that can follow upon abnormalities of centrosome number and of the segregation of chromosomes, he associated causally the already known phenomenon of centrosome abnormalities of cancer with the latter's histopathology. He further posited that such pathology could be attributed to a single chromosomally aberrant cell.
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[
Seminars in Developmental Biology,
1992]
At the 4-cell stage of the C. elegans embryo, three axes can be defined: anterior-posterior (A-P), dorsal-ventral (D-V), and left-right (L-R). The A-P axis first becomes obvious in the newly fertilized 1-cell embryo. Pronouned cytoplasmic assymmetries arise along the A-P axis during the first cell cycle, after which the zygote undergoes a series of stem cell-like cleavages with an A-P orientation of the mitotic spindle; these cleavages generate several somatic founder cells and a primordial germ cell. The D-V and L-R axes are defined by the direction of spindle rotation as the 2-cell embryo divides into four cells. In contrast to the A-P axis, there do not appear to be cellular asymmetries associated with the D-V and L-R axes, and both axes can easily be reversed by micromanipulation. Thus, with respect to the roles that the embryonic axes serve in cell-fate determination in the early C. elegans embryo, it appears that internally transmitted developmental information is differentially segregated along the A-P axis, but not along the D-V or L-R axes. Instead, D-V and L-R differences in the fates of cells within lineages appear to be dictated by differential
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[
J Leukoc Biol,
1996]
The recognition that apoptosis is regulated by an evolutionarily conserved set of polypeptides from the nematode Caenorhabditis elegans to humans suggests that a conserved set of biochemical mechanisms may also he involved in the response. Work from a number of independent laboratories suggests that alterations in cytosolic Ca2+ homeostasis represent one such candidate mechanism, and molecular targets for Ca2+ are now being identified. This review will summarize what is known about the role of Ca2+ in the regulation of apoptosis and discuss how Ca2+ might interact with some of the other biochemical signals implicated in cell death.
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[
Cell Microbiol,
2018]
Legionella pneumophila is a ubiquitous environmental bacterium that has evolved to infect and proliferate within amoebae and other protists. It is thought that accidental inhalation of contaminated water particles by humans is what has enabled this pathogen to proliferate within alveolar macrophages and cause pneumonia. However, the highly evolved macrophages are equipped more sophisticated innate defense mechanisms than protists, such as the evolution of phagotrophic feeding into phagocytosis with more evolved innate defense processes. Not surprisingly, the majority of proteins involved in phagosome biogenesis (~80%) have origins in the phagotrophy stage of evolution. There are a plethora of highly evolved cellular and innate metazoan processes, not represented in Protist biology, that are modulated by L. pneumophila; including TLR2 signaling, NF-B, apoptotic and inflammatory processes, histone modification, caspases, and the NLRC-Naip5 inflammasomes. Importantly, L. pneumophila infects hemocytes of the invertebrate Galleria mellonella, kill G. mellonella larvae, and proliferate in and kill Drosophila adult flies and Caenorhabditis elegans. Although co-evolution with protist hosts has provided a substantial blueprint for L. pneumophila to infect macrophages, we discuss the further evolutionary aspects of co-evolution of L. pneumophila and its adaptation to modulate various highly evolved innate metazoan processes prior to becoming a human pathogen.