nhr-25, the Caenorhabditis elegans Ortholog of ftz-f1, Is Required for Epidermal and Somatic Gonad Development

Abstract

We have analyzed the expression and function of the Caenorhabditis elegans gene nhr-25, a member of the widely conserved FTZ-F1 family of nuclear receptors. The gene encodes two protein isoforms, only one of which has a DNA binding domain. nhr-25 is transcribed during embryonic and larval development. A nhr-25::GFP fusion gene is expressed in the epidermis, the developing somatic gonad, and a subset of other epithelial cells. RNA-mediated interference indicates a requirement for nhr-25 function during development: disruption of nhr-25 function leads to embryonic arrest due to failure of the epidermally mediated process of embryo elongation. Animals that survive to hatching arrest as misshapen larvae that occasionally exhibit defects in shedding molted cuticle. In addition, somatic gonad development is defective in these larvae. These results further establish the importance of FTZ-F1 nuclear receptors in molting and developmental control across evolutionarily distant phyla.

The Caenorhabditis elegans Cathepsin Z-like Cysteine Protease, Ce-CPZ-1, Has a Multifunctional Role during the Worms' Development

“…Interestingly, inhibition of nhr-23, nhr-25, and lrp-1 gene expression also resulted in some morphological abnormalities. All these genes, including cpz-1, are highly expressed in the major hypodermal cells in all larval stages of nematodes, which supports their involvement in epidermal differentiation during or after molting (45,46,48).…”

“…Control mechanisms that regulate such a complicated process are poorly understood, but recent studies have implicated two C. elegans nuclear hormone receptors (NHR-23 and NHR-25) in the regulation of molting (45)(46)(47). Molting defects were observed after interference with C. elegans nhr-25 gene expression by RNAi.…”

Thehedgehog-related genequa-1 is required for molting inCaenorhabditis elegans

“…qua-1(gk32) causes developmental arrests at the L1/L2 stage with a high penetrance (98%). This early arrest is in contrast to other molting mutants such as lrp-1, nhr-23, and nhr-25 that exhibit molting defects in all four larval stages (Kostrouchova et al, 1998;Yochem et al, 1999;Gissendanner and Sluder, 2000). Observation of the arrested qua-1 mutant larvae reveals that molting is defective.…”

“…So far, the regulatory mechanisms of C. elegans molting are not yet understood, although about a dozen genes have been identified that lead to molting defects when mutated. These genes can be classified into five categories based on their possible functions: (1) proteases that are used to degrade the old cuticle, including a cathepsin Z-like cysteine protease (Cecpz-1) (Hashmi et al, 2004), and two metalloproteases, nas-36 and nas-37 (Davis et al, 2004;Suzuki et al, 2004); (2) transcriptional regulators, including nhr-23 (Kostrouchova et al, 1998(Kostrouchova et al, , 2001, nhr-25 (Asahina et al, 2000;Gissendanner and Sluder, 2000), and let-19 (Wang et al, 2004); (3) enzymes involved in cholesterol metabolism such as let-767 (Kuervers et al, 2003) or cholesterol transporters such as lrp-1 (Yochem et al, 1999); (4) molecules involved in secretion and extracellular transport such as sec-23 (Roberts et al, 2003) and CeVps-27 (Roudier et al, 2005); (5) others, such as the angiotensin converting enzyme-like non-peptidase acn-1 (Brooks et al, 2003).…”

Nuclear receptor BgFTZ‐F1 regulates molting and the timing of ecdysteroid production during nymphal development in the hemimetabolous insect Blattella germanica

“…As observed in insects, expression of nhr-23 and nhr-25 mRNAs oscillates with each molting cycle (Gissendanner et al, 2004) and RNAi of both receptors at the intermolt results in a defective molt, with associated problems of cuticle shedding (Ashaina et al, 2000;Gissendanner and Sluder, 2000). However, whereas HR3 controls the expression of FTZ-F1 in insects, nhr-25 expression seems not dependent of nhr-23 (Krostrouchova et al, 2001).…”