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[
2020]
Onchocerciasis, also known as the African river blindness, is the second most important cause of infectious blindness worldwide after trachoma. It is caused by the filarial nematode, <i>Onchocerca volvulus</i>, and transmitted by repeated bites of the vector, female black fly of the genus <i>Simulium damnosum</i>. The vector breeds in fast-flowing and oxygen-rich rivers in affected areas with transmission and disease prevalence usually stretching along these river basins and thereby the name river blindness.[1]Aside from blindness, onchocerciasis results in a troubling chronic dermatitis.[1]
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[
WormBook,
2006]
In the last decade, nematodes other than C. elegans have been studied intensively in evolutionary developmental biology. A few species have been developed as satellite systems for more detailed genetic and molecular studies. One such satellite species is the diplogastrid nematode Pristionchus pacificus. Here, I provide an overview about the biology, phylogeny, ecology, genetics and genomics of P. pacificus.
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[
2008]
Germline stem cells (GSCs) can generate haploid gametes, sperms or oocyte, which are responsible for transmitting genetic information from generation to generation. Because GSCs can be easily identified and gene functions can be readily manipulated in Drosophila and C. elegans, their niches were among the first to be functionally and anatomically defined. Genetic and cell biological studies in these systems have first shown that stem cell function is controlled by extracellular cues from the niche, and intrinsic genetic programs within the stem cells. Important progress has also recently been made in localizing GSCs in the mouse testis. Here I will review recent progress and compare the differences and commonalities of GSC niches from different systems. Since the studies on GSC niches in Drosophila and C. elegans have provided guiding principles for initial identification of niches in other systems, I hope that this review will provide some stimulating thoughts about niche structures and functions of adult stem cells in somatic systems.
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[
WormBook,
2007]
The C. elegans foregut (pharynx) has emerged as a powerful system to study organ formation during embryogenesis. Here I review recent advances regarding cell-fate specification and epithelial morphogenesis during pharynx development. Maternally-supplied gene products function prior to gastrulation to establish pluripotent blastomeres. As gastrulation gets under way, pharyngeal precursors become committed to pharyngeal fate in a process that requires PHA-4 /FoxA and the Tbox transcription factors TBX-2 , TBX-35 , TBX-37 and TBX-38 . Subsequent waves of gene expression depend on the affinity of PHA-4 for its target promoters, coupled with combinatorial strategies such as feed-forward and positive-feedback loops. During later embryogenesis, pharyngeal precursors undergo reorganization and a mesenchymal-to-epithelial transition to form the linear gut tube. Surprisingly, epithelium formation does not depend on cadherins, catenins or integrins. Rather, the kinesin ZEN-4 /MKLP1 and CYK-4 /RhoGAP are critical to establish the apical domain during epithelial polarization. Finally, I discuss similarities and differences between the nematode pharynx and the vertebrate heart.
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[
1976]
The genetics of a small, free-living nematode, Caenorhabditis elegans, has been utilized recently to characterize many mutants affecting the development, function and structure of nerve and muscle. A number of mutants induced by ethyl methane sulfonate (EMS) have been discovered and specifically disrupt the myofibrillar elements of body wall muscle cells, leading to paralysis. One of these mutants, E675, produces an abnormal myosin heavy chain in body wall muscles. Several other mutants as well as E675 are the results of mutation within
unc-54, a gene on chromosome I....
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[
1977]
The soil nematode Caenorhabditis elegans was selected 11 years ago by Sydney Brenner as an experimental organism suitable for the isolation of many behavioral mutants and small enough for anatomical analysis of such mutants with the electron microscope. Two distinct goals motivated the initial studies of this organism: first, the hope that some of the mutants would have simple anatomical alterations that could be directly correlated with their behavioral defects, allowing the assignment of specific functions to specific neurons, and second, the hope that the detailed analysis of the kinds of alterations induced by individual mutations and the classes of cells affected by given mutations would reveal general features of the genetic program that specifies the development of the organism. Over the past 11 years the number of investigators working on C. elegans has increased to about 75 and is still growing. Nearly 3,000 different mutants have been isolated and different investigators are pursuing their effects on different cells. My own research is in the development of the nervous system. In particular, I would like to learn something about the workings of the complex black box that connects individual genes to the determination of the morphology of developing neurons. Are there gene products whose specific function is to determine the morphology of cells? If so, what are these gene products and how do they act in the developing cell? One would anticipate that mutations in such hypothetical genes would cause specific morphological alterations in cells. Because the morphology of a neuron determines its function, by selecting behavioral mutants altered in the function of the nervous system one might commonly find mutants that alter the morphology of neurons, and some of these might be in specific morphological genes. It is my hope that it will be possible to compare such mutants to the wild type in order to identify the defective gene products and thereby learn something about the role of normal gene products in determining the development of neurons. In this paper I will first summarize the results of several years' work on one specific class of mutants in the nematode, sensory mutants, work performed both in my laboratory and that of my colleagues Jim Lewis and Jonathan Hodgkin. Second, I will discuss frankly some of the difficulties and frustrations we have experienced in trying to interpret the effects of these specific mutants. Some of these difficulties illustrate problems endemic to genetic studies of development. Third, I will describe the more recent work performed in my labortory that is being directed toward genetic analysis of the structure and function of a
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[
1987]
To my knowledge, a theory of "developmentally programmed aging" has never been explicitly stated, although the notion that aging has some relationship to development has certainly been proposed many times. In the preceding chapter (36), Dr. Hayflick has made a brief description of the central idea of developmental programming within aging. In order to discuss relevant evidence in this chapter, I would like to propose the following, somewhat more specific and operational definition: The theory of developmentally programmed aging posits that aging involves events controlled in ways recognizably similar to those that operate during development. This definition is perhaps a little less extreme than it might have been, since it uses the phrase "aging involves events" rather than the phrase "aging is caused by events." However, I think it captures most of the usual connotations of "developmentally programmed aging," and it at least has the virtue of testability. Of course, to test the theory, as defined, requires evidence of several sorts. In particular, it requires (a) that we understand how some aging events are controlled, (b) that we understand how some developmental events are controlled, and (c) that we know how to recognize whether there is or is not similarity between the two. A central message of what follows is that we are really only at the beginning of being able to test this theory, although some lines of approach do appear
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[
1983]
Most multicellular eukaryotes posses a distinct group of germ-line cells that produces oocytes in one sex and sperm in the other. The production of adult germ cells appears to involve several developmental steps. First, during early embryogenesis, one or a few cells are committd to become germ precursor cells. Secondly, after a period of proliferation, some or all germ line descendants of the germ precursor cell leave the mitotic cell cycle and enter meiotic prophase. Thirdly, the meiotic germ cell matures as either a sperm or an oocyte. In this paper, I will review our knowledge of how each of these steps might be controlled in the small non-parasitic soil nematode, Caenorhabditis elegans.
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[
1960]
I would like to introduce my lecture on this subject with a brief consideration of meiosis in the female. The oogonial cells in the anterior part of the ovary in a nematode are small and multiply by mitosis. As they move down the ovary they increase in size with corresponding increase in the size of the nucleus. The chromatin is a single spherical mass located in the center of the nucleus. Eventually the chromatin mass is resolved into individual chromosomes. During prophase of meiosis the homologous chromosomes come together. All diploid cells possess identical chromosomes with the exception of the sex chromosomes and at synapsis these homologous chromosomes pair or come together. Paternal and maternal gametes each contribute a complement of identical chromosomes.
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[
WormBook,
2005]
Nematodes are the most abundant type of animal on earth, and live in hot springs, polar ice, soil, fresh and salt water, and as parasites of plants, vertebrates, insects, and other nematodes. This extraordinary ability to adapt, which hints at an underlying genetic plasticity, has long fascinated biologists. The fully sequenced genomes of Caenorhabditis elegans and Caenorhabditis briggsae, and ongoing sequencing projects for eight other nematodes, provide an exciting opportunity to investigate the genomic changes that have enabled nematodes to invade many different habitats. Analyses of the C. elegans and C. briggsae genomes suggest that these include major changes in gene content; as well as in chromosome number, structure and size. Here I discuss how the data set of ten genomes will be ideal for tackling questions about nematode evolution, as well as questions relevant to all eukaryotes.