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Development,
2021]
Swathi Arur is an Associate Professor for the Department of Genetics at the MD Anderson Cancer Center, USA, where she uses multidisciplinary approaches to understand female germline development and fertility. She has received numerous accolades, including the MD Anderson Distinguished Research Faculty Mentor Award in 2017. In 2020, she was elected to the American Association for the Advancement of Science (AAAS). Swathi joined the team at Development as an Academic Editor in 2020, and we met with her over Zoom to hear more about her life, her career and her love for <i>C. elegans</i>.
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Dev Cell,
2019]
In this issue of Developmental Cell, Anderson etal. (2019) show that chromatin domain structure on the X chromosome in C.elegans is dispensable for dosage compensation but regulates longevity and thermotolerance. This study sheds light on the mechanisms of domain formation in C.elegans and how these features affect physiology.
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MicroPubl Biol,
2022]
Caenorhabditis elegans is a model species, increasingly used in experimental evolution studies to investigate such major topics as: maintenance of genetic variation, host-pathogen interaction and coevolution, mutations, life history, evolution of reproductive systems, sexual selection (Gray and Cutter, 2014; Teotnio, Estes, Phillips, and Baer, 2017). Its reproductive system in the wild, known as androdioecy, involves mostly self-fertilization of hermaphrodites and occasionally outcrossing with males, which are generally rare (Stewart and Phillips, 2002). This system can be experimentally changed to dioecy, i.e., obligatory outcrossing, through genetic manipulations (see Table I in Anderson, Morran, and Phillips, 2010; Gray and Cutter, 2014).
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Nematologica,
1969]
Several investigators have reported that nutritional or environmental factors induce morphological variations in the "so-called' bacteriophagous nematodes. For example, Nigon & Dougherty described a morphological mutant of the free-living, self-fertilizing, hermaphroditic nematode Rhabditis (Caenorhabditis) briggsae that ensued following heat-treatment of progeny cultured on bacteria. Also Anderson reported that certain diagnostic features of an Acrobeloides sp., specifically the shape of the labial probolae and tail, varied significantly when the nematodes were grown on bacterial cultures as compared to those grown in soil. The current paper describes a consistent morphological variation in Caenorhabditis briggsae grown axenically on a meridic medium containing a growth factor from a bacterium as compared with nematodes reared on a growth factor from liver extract.
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Fundamental and Applied Nematology,
1997]
The effects of structural heterogeneity on both chemical diffusion and nematode movement are examined with the development of a theoretical model. The model considers three factors affecting nematode movement: soil structure, nematode foraging strategy and chemotaxis. Using a continuous model, we develop a discrete system which allows nematode trails to be simulated in any of the four experimental conditions given by Anderson et al (1997). We show that structural heterogeneity causes mixed levels of attractant concentration over small areas as well as "fingering" of the attractant. Soil structural heterogeneity also restricts the foraging strategy of the nematode which then becomes a strategy to avoid structural "traps". The effect of localised increases in structural density is shown to increase significantly "fingering" of the attractant.
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Bio Protoc,
2017]
Eukaryotic cells contain various types of cytoplasmic, non-membrane bound ribonucleoprotein (RNP) granules that consist of non-translating mRNAs and a versatile set of associated proteins. One prominent type of RNP granules are Processing bodies (P bodies), which majorly harbors translationally inactive mRNAs and an array of proteins mediating mRNA degradation, translational repression and cellular mRNA transport (Sheth and Parker, 2003). Another type of RNP granules, the stress granules (SGs), majorly contain mRNAs associated with translation initiation factors and are formed upon stress-induced translational stalling (Kedersha et al., 2000 and 1999). Multiple evidence obtained from studies in unicellular organisms supports a model in which P bodies and SGs physically interact during cellular stress to direct mRNAs for transport, decay, temporal storage or reentry into translation (Anderson and Kedersha, 2008; Decker and Parker, 2012). The quantification, distribution and colocalization of P bodies and/or SGs are essential tools to study the composition of RNP granules and their contribution to fundamental cellular processes, such as stress response and translational regulation. In this protocol we describe a method to quantify P bodies and SGs in somatic tissues of the nematode Caenorhabditis elegans.
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Mol Cell Biol,
2010]
Prolonged cellular hypoxia results in energy failure and ultimately cell death. However, less-severe hypoxia can induce a cytoprotective response termed hypoxic preconditioning (HP). The unfolded protein response pathway (UPR) has been known for some time to respond to hypoxia and regulate hypoxic sensitivity; however, the role of the UPR, if any, in HP essentially has been unexplored. We have shown previously that a sublethal hypoxic exposure of the nematode Caenorhabditis elegans induces a protein chaperone component of the UPR (L. L. Anderson, X. Mao, B. A. Scott, and C. M. Crowder, Science 323:630-633, 2009). Here, we show that HP induces the UPR and that the pharmacological induction of misfolded proteins is itself sufficient to stimulate a delayed protective response to hypoxic injury that requires the UPR pathway proteins IRE-1, XBP-1, and ATF-6. HP also required IRE-1 but not XBP-1 or ATF-6; instead, GCN-2, which is known to suppress translation and induce an adaptive transcriptional response under conditions of UPR activation or amino acid deprivation, was required for HP. The phosphorylation of the translation factor eIF2, an established mechanism of GCN-2-mediated translational suppression, was not necessary for HP. These data suggest a model where hypoxia-induced misfolded proteins trigger the activation of IRE-1, which along with GCN-2 controls an adaptive response that is essential to HP.