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[
Cell Calcium,
2011]
IP receptor is a Ca(2+) release channel localized on the endoplasmic reticulum. IP(3) receptor is composed of three isoforms, which are expressed in various cells and tissues, and play variety of roles throughout development. I here describe the role of IP receptor from oogenesis, meiotic maturation and fertilization. I also describe the Ca(2+) signaling at meiosis and mitosis, and especially the role in early embryogenesis to determine dorso-ventral axis formation. Loss of function mutation of type 1 IP receptor in mouse, both by gene targeting and spontaneous mutations shows severe ataxia and other phenotypes. Interestingly, double knockouts of type 1 and type 2 exhibit cardiogenesis arrest and that of type 2 and type 3 results in exocrine secretion deficit. IPR of Drosophila or Caenorhabditis elegans is single gene and mutation results severe phenotype of behavior. All the data described here show that IPRs are essential for life and abnormality of IP(3)Rs results in severe abnormality in its structure and function of organism.
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Curr Biol,
2000]
Recent studies of vulva development in the nematode Pristionchus pacificus have identified cell interactions that do not appear to occur in Caenorhabditis elegans, The new results underscore the diversity of patterning mechanisms that can produce structures with similar cellular morphology.
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Curr Biol,
2001]
How do animal tissues resist the shearing forces to which they are exposed during locomotion or harsh encounters with the environment? Genetic analysis in Caenorhabditis elegans is furthering our understanding of the nature and function of the attachments that preserve tissue integrity.
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Trends Biochem Sci,
2002]
The partitioning of cells by a nuclear envelope ensures that precursors of ribosomes do not interact prematurely with other components of the translation machinery. Ribosomal subunits are assembled in nucleoli and exported to the cytoplasm in a CRM1/Ran-GTP-dependent fashion. Export of the large (60S) subunit requires a shuttling adaptor protein, NMD3, which binds to mature, correctly folded subunits. Immature or defective particles do not bind NMD3 and thus are excluded from the export pathway. This structural proofreading is extended into the cytoplasm, where it is believed that several energy-requiring steps release shuttling factors from the subunit, allowing it to function in translation.
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Metallomics,
2014]
Phytochelatins are sulfur-rich metal-binding peptides, and phytochelatin synthesis is one of the key mechanisms by which plants protect themselves against toxic soft metal ions such as cadmium. It has been known for a while now that some invertebrates also possess functional phytochelatin synthase (PCS) enzymes, and that at least one species, the nematode Caenorhabditis elegans, produces phytochelatins to help detoxify cadmium, and probably also other metal and metalloid ions including arsenic, zinc, selenium, silver, and copper. Here, we review recent studies on the occurrence, utilization, and regulation of phytochelatin synthesis in invertebrates. The phytochelatin synthase gene has a wide phylogenetic distribution, and can be found in species that cover almost all of the animal tree of life. The evidence to date, though, suggests that the occurrence is patchy, and even though some members of particular taxonomic groups may contain PCS genes, there are also many species without these genes. For animal species that do possess PCS genes, some of them (e.g. earthworms) do synthesize phytochelatins in response to potentially toxic elements, whereas others (e.g. Schistosoma mansoni, a parasitic helminth) do not appear to do so. Just how (and if) phytochelatins in invertebrates complement the function of metallothioneins remains to be elucidated, and the temporal, spatial, and metal specificity of the two systems is still unknown.
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Int J Parasitol,
1996]
Most nematode messenger RNAs (mRNAs) have at their 5' end a common 22 nucleotide leader sequence, the trans-spliced leader or SL1. The presence of this leader on some but not all mRNAs raises several questions: What is the role of the spliced leader in mRNA maturation, stability and translation? Why do some genes have a spliced leader and others not? What is the evolutionary origin of this trans-splicing mechanism? Recently, additional trans-spliced leaders (SL2, 3, 4, 5) have been described. What role do these variants play in nematode gene expression? While definitive answers to these questions remain elusive, it is clear that the spliced leader will significantly facilitate the cloning and sequence analysis of most nematode mRNAs.
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Cell Calcium,
2007]
The nematode Caenorhabditis elegans provides numerous experimental advantages for developing an integrative molecular understanding of physiological processes and has proven to be a valuable model for characterizing Ca(2+) signaling mechanisms. This review will focus on the role of Ca(2+) release activated Ca(2+) (CRAC) channel activity in function of the worm gonad and intestine. Inositol 1,4,5-trisphosphate (IP(3))-dependent oscillatory Ca(2+) signaling regulates contractile activity of the gonad and rhythmic posterior body wall muscle contraction (pBoc) required for ovulation and defecation, respectively. The C. elegans genome contains a single homolog of both STIM1 and Orai1, proteins required for CRAC channel function in mammalian and Drosophila cells. C. elegans STIM-1 and ORAI-1 are coexpressed in the worm gonad and intestine and give rise to robust CRAC channel activity when coexpressed in HEK293 cells. STIM-1 or ORAI-1 knockdown causes complete sterility demonstrating that the genes are essential components of gonad Ca(2+) signaling. Knockdown of either protein dramatically inhibits intestinal cell CRAC channel activity, but surprisingly has no effect on pBoc, intestinal Ca(2+) oscillations or intestinal ER Ca(2+) store homeostasis. CRAC channels thus do not play obligate roles in all IP(3)-dependent signaling processes in C. elegans. Instead, we suggest that CRAC channels carry out highly specialized and cell specific signaling roles and that they may function as a failsafe mechanism to prevent Ca(2+) store depletion under pathophysiological and stress conditions.
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Methods Cell Biol,
1995]
This chapter has two aims. First, we describe one method, the electropharyngeogram (EPG), insufficient detail that a Caenorhabditis elegans researcher unfamiliar with electrophysiological methods could set up the apparatus and get useful results. Second, we describe more generally for researchers familiar with electrophysiological methods how they may be applied to C. elegans. We do not describe methods for electrophysiological investigation of C. elegans sperm.
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[
Cell,
1992]
How sister cells have different fates is a fundamental aspect of the problem of how cell diversity is generated during development. In principle, sister cells that are different could be produced in two distinct ways. First, polar mother cells could divide to generate daughters that are different from the time they are formed. Alternatively, two identical sisters could be generated and become different as a consequence of some later event. Consideration of these mechansisms raises immediate further questions: What causes a mother cell to be polar? How do initially identical sister cells become different? And in each case, how do initial differences in sister cells lead to their ultimately distinct fates? Answers to these questions would provide important insights into the mechanisms responsible for the control of development. In this review we use the term "asymmetric cell division" to refer to any cell division in which sister cells have different fates...
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Cell,
2005]
A cost of reproduction, where lifespan and fecundity are negatively correlated, is of widespread occurrence. Mutations in insulin/IGF signaling (IIS) pathways and dietary restriction (DR) can extend lifespan in model organisms but do not always reduce fecundity, suggesting that the link between lifespan and fecundity is not inevitable. Understanding the molecular basis of the cost of reproduction will be informed by elucidation of the mechanisms by which DR and IIS affect these two traits.