Genetic Models of Mechanotransduction: The Nematode<i>Caenorhabditis elegans</i>

Syntichaki, Popi; Tavernarakis, Nektarios

doi:10.1152/physrev.00043.2003

Cited by 116 publications

(109 citation statements)

References 471 publications

(1,064 reference statements)

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“…22) Agesynchronized worms were used in all assays, and they were obtained after alkaline hypochlorite treatment of hermaphrodites. 23) To prepare treatment plates, ECH was first dissolved in sterilized distilled water, and subsequently, this stock solution was inserted into autoclaved NGM plates at 55°C to the indicated final concentrations. 24,25) For ECH-treated assays, heatinactivated OP50 (65°C for 30 min) was utilized to prevent ECH metabolized by E. coli.…”

Section: Worms Maintenance and Ech Treatmentmentioning

confidence: 99%

The longevity effect of echinacoside inCaenorhabditis elegansmediated throughdaf-16

Wang

Zhang

Liu

et al. 2015

Bioscience, Biotechnology, and Biochemistry

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Echinacoside (ECH), a natural polyphenolic compound, has been reported to possess important pharmacological activities. However, very little is known about whether or how ECH affects longevity in vivo. We have examined the effects of ECH on the life span and stress tolerance in Caenorhabditis elegans. Our studies demonstrate that the life span of wild-type worms could be extended in the presence of ECH. Furthermore, ECH was found to increase tolerance of worms to heat shock and oxidative stress, while not exerting any influence on pharyngeal pumping rate and progeny production. Our mechanistic studies indicate that supplementation of ECH increases the transcript level of daf-16. ECH treatment also modulates the nuclear localization and transcriptional activities of daf-16, thus fine tunes the expression of daf-16 target genes to promote longevity and increases stress response in C. elegans. Overall, this work reveals the longevity effect of ECH and elucidates the underpinning mechanisms.

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Section: Worms Maintenance and Ech Treatmentmentioning

confidence: 99%

The longevity effect of echinacoside inCaenorhabditis elegansmediated throughdaf-16

Wang

Zhang

Liu

et al. 2015

Bioscience, Biotechnology, and Biochemistry

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“…2). Of the 89 homeodomain proteins encoded by the C. elegans genome (Okkema and Krause, 2005), CEH-51 is most closely related to CEH-7 (Kagoshima et al, 1999), CEH-24 (Harfe and Fire, 1998) and TAB-1 (CEH-29) [L. Carnell and M. Chalfie, unpublished data cited in Syntichaki and Tavernarakis (Syntichaki and Tavernarakis, 2004)], sharing 41-48% identity (57-58% similarity) within the homeodomain (Fig. 2B,C).…”

Section: Identification Of Ceh-51 a Putative Nk-2 Class Homeodomain mentioning

confidence: 99%

The NK-2 class homeodomain factor CEH-51 and the T-box factor TBX-35 have overlapping function inC. elegansmesoderm development

et al. 2009

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The C. elegans MS blastomere, born at the 7-cell stage of embryogenesis, generates primarily mesodermal cell types, including pharynx cells, body muscles and coelomocytes. A presumptive null mutation in the T-box factor gene tbx-35, a target of the MED-1 and MED-2 divergent GATA factors, was previously found to result in a profound decrease in the production of MS-derived tissues, although the tbx-35(-) embryonic arrest phenotype was variable. We report here that the NK-2 class homeobox gene ceh-51 is a direct target of TBX-35 and at least one other factor, and that CEH-51 and TBX-35 share functions. Embryos homozygous for a ceh-51 null mutation arrest as larvae with pharynx and muscle defects, although these tissues appear to be specified correctly. Loss of tbx-35 and ceh-51 together results in a synergistic phenotype resembling loss of med-1 and med-2. Overexpression of ceh-51 causes embryonic arrest and generation of ectopic body muscle and coelomocytes. Our data show that TBX-35 and CEH-51 have overlapping function in MS lineage development. As T-box regulators and NK-2 homeodomain factors are both important for heart development in Drosophila and vertebrates, our results suggest that these regulators function in a similar manner in C. elegans to specify a major precursor of mesoderm.

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“…Note that both nematode and vertebrate have a shaker-type channel associated with the mechanosensory channel, but details are unknown. Modified after (Bryant et al, 2005, Chiang et al, 2004, Syntichaki and Tavernarakis, 2004.…”

Section: Molecular Evolution Suggests Conservation Of Tethers But Nomentioning

confidence: 99%

Molecular evolution of the vertebrate mechanosensory cell and ear

Fritzsch¹,

Beisel²,

Pauley³

et al. 2007

Int. J. Dev. Biol.

101

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The molecular basis of mechanosensation, mechanosensory cell development and mechanosensory organ development is reviewed with an emphasis on its evolution. In contrast to eye evolution and development, which apparently modified a genetic program through intercalation of genes between the master control genes on the top (Pax6, Eya1, Six1) of the hierarchy and the structural genes (rhodopsin) at the bottom, the as yet molecularly unknown mechanosensory channel precludes such a firm conclusion for mechanosensors. However, recent years have seen the identification of several structural genes which are involved in mechanosensory tethering and several transcription factors controlling mechanosensory cell and organ development; these warrant the interpretation of available data in very much the same fashion as for eye evolution: molecular homology combined with potential morphological parallelism. This assertion of molecular homology is strongly supported by recent findings of a highly conserved set of microRNAs that appear to be associated with mechanosensory cell development across phyla. The conservation of transcription factors and their regulators fits very well to the known or presumed mechanosensory specializations which can be mostly grouped as variations of a common cellular theme. Given the widespread distribution of the molecular ability to form mechanosensory cells, it comes as no surprise that structurally different mechanosensory organs evolved in different phyla, presenting a variation of a common theme specified by a conserved set of transcription factors in their cellular development. Within vertebrates and arthropods, some mechanosensory organs evolved into auditory organs, greatly increasing sensitivity to sound through modifications of accessory structures to direct sound to the specific sensory epithelia. However, while great attention has been paid to the evolution of these accessory structures in vertebrate fossils, comparatively less attention has been spent on the evolution of the inner ear and the central auditory system. Recent advances in our molecular understanding of ear and brain development provide novel avenues to this neglected aspect of auditory neurosensoy evolution.

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Genetic Models of Mechanotransduction: The NematodeCaenorhabditis elegans

Cited by 116 publications

References 471 publications

The longevity effect of echinacoside inCaenorhabditis elegansmediated throughdaf-16

The longevity effect of echinacoside inCaenorhabditis elegansmediated throughdaf-16

The NK-2 class homeodomain factor CEH-51 and the T-box factor TBX-35 have overlapping function inC. elegansmesoderm development

Molecular evolution of the vertebrate mechanosensory cell and ear

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