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Ultradian rhythm in the intestine of Caenorhabditis elegans is controlled by the C‐terminal region of the FLR‐1 ion channel and the hydrophobic domain of the FLR‐4 protein kinase

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TLDR
It is shown that a truncated FLR‐1 lacking the C‐terminal intracellular region resulted in longer periods, suggesting that this region is involved in the negative regulation of defecation cycle periods.
Abstract
Defecation behavior in Caenorhabditis elegans is driven by an endogenous ultradian clock in the intestine. Its periods are positively regulated by FLR-1, an ion channel of the epithelial sodium channel/degenerin superfamily, and FLR-4, a protein kinase with a hydrophobic domain at the carboxyl terminus. FLR-1 has many putative phosphorylation sites in the C-terminal intracellular region. This structure implies that the periods may be regulated by the phosphorylation of FLR-1 by FLR-4, but it remains to be clarified. Here, we show that a truncated FLR-1 lacking the C-terminal intracellular region resulted in longer periods, suggesting that this region is involved in the negative regulation of defecation cycle periods. Contrary to our expectation, FLR-4 was still necessary for the function of the truncated FLR-1. Furthermore, FLR-4 containing a kinase-dead mutation or lacking the whole kinase domain was sufficient for normal defecation cycle periods. FLR-4 was necessary for the stable expression of FLR-1::GFP, and its hydrophobic domain was sufficient also for this function. FLR-1 and FLR-4 are often colocalized in the plasma membrane. These data showed an unexpected role of FLR-4: its hydrophobic domain stabilizes the FLR-1 ion channel, a key regulator of defecation cycle periods in the intestine.

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Journal ArticleDOI

An N-myristoylated globin with a redox-sensing function that regulates the defecation cycle in Caenorhabditis elegans.

TL;DR: This work proposes a function for a membrane-bound globin of C. elegans, GLB-26, predicted to be myristoylated at its N-terminus, a post-translational modification only recently described in the globin family.
Journal ArticleDOI

Distinct roles for two Caenorhabditis elegans acid-sensing ion channels in an ultradian clock

- 06 Jun 2022 - 
TL;DR: Kaulich et al. as discussed by the authors identified two acid-sensing ion channels, with very different proton sensing properties, and described their role in an ultradian clock, the defecation motor program (DMP) of the nematode Caenorhabditis elegans.
Journal ArticleDOI

The Doubletime Homolog KIN-20 Mainly Regulates let-7 Independently of Its Effects on the Period Homolog LIN-42 in Caenorhabditis elegans .

TL;DR: It is found that kin-20 RNAi enhances loss-of-function lin-42 mutant phenotypes and that Kin-20 mutant worms express lower levels of LIN-42 and let-7 microRNAs, and it is suggested that thoughKin-20 regulates lin-41 and let's7 microRNA, it mainly affects let- 7 microRNA expression independently of lin- 42.
Posted ContentDOI

Distinct roles for two Caenorhabditis elegans acid-sensing ion channels in an ultradian clock

TL;DR: In this article, the authors identify two acid-sensing ion channels, with very different proton sensing properties, and describe their role in an ultradian clock, the defecation motor program (DMP) of the nematode Caenorhabditis elegans.
Posted ContentDOI

Follicle stimulating hormone signaling opposes the DRL-1/FLR-4 MAP Kinases to balance p38-mediated growth and lipid homeostasis in C. elegans

TL;DR: In this paper , a forward genetic screen for suppressors of the drl-1 mutant phenotypes and identified mutations in flr-2 and fshr-1, which encode the orthologues of follicle stimulating hormone and its putative G protein-coupled receptor, respectively.
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Journal ArticleDOI

WW domains of Nedd4 bind to the proline-rich PY motifs in the epithelial Na+ channel deleted in Liddle's syndrome.

TL;DR: The results demonstrate that the WW domains of rNedd4 bind to the PY motifs deleted from beta or gammaENaC in Liddle's syndrome patients, and suggest that Nedd4 may be a regulator (suppressor) of the epithelial Na+ channel.