500+ Papers found (0.013 seconds)

Branicky R et al. (2000) Bioessays "clk-1, mitochondria, and physiological rates."

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Bioessays,

2000]

Mutations in the C. elegans maternal-effect gene clk-1 are highly pleiotropic, affecting the duration of diverse developmental and behavioral processes. They result in an average slowing of embryonic and post-embryonic development, adult rhythmic behaviors, reproduction, and aging.(1) CLK-1 is a highly conserved mitochondrial protein,(2,3) but even severe clk-1 mutations affect mitochondrial respiration only slightly.(3) Here, we review the evidence supporting the regulatory role of clk-1 in physiological timing. We also discuss possible models for the action of CLK-1, in particular, one proposing that CLK-1 is involved in the coordination of mitochondrial and nuclear function. BioEssays 22:48-56, 2000.

Ji YJ et al. (2005) J Cell Biochem "RNT-1 regulation in C. elegans."

Singaravelu G, Ji YJ, Ahnn J

[

J Cell Biochem,

2005]

RUNXs are important transcription factors, which are involved in animal development and human carcinogenesis. RNT-1, the only homologue of RUNXs, in Caenorhabditis elegans (C. elegans) has been identified and viable mutant animals of rnt-1 gene have been isolated and characterized recently. Genetic analyses using rnt-1 mutants have shown that RNT-1 is regulated by TGFbeta- and Wnt-signaling pathways in the body size regulation and male tail development. Here, we review our current understanding of RNT-1 functions in these signaling pathways. Furthermore, future prospects of RNT-1 and BRO-1 studies in C. elegans are discussed in this review. (c) 2005 Wiley-Liss, Inc.

Passananti C et al. (2007) Biochem Cell Biol "Che-1/AATF, a multivalent adaptor connecting transcriptional regulation, checkpoint control, and apoptosis."

Passananti C, Fanciulli M, Floridi A

[

Biochem Cell Biol,

2007]

Che-1/AATF (Che-1) was originally characterized as an interacting protein for RNA polymerase II. In addition to transcriptional regulation, the evidence suggests that Che-1 has a viral factor-like S phase promoting role in counteracting Rb repression to facilitate E2F-dependent transactivation during G1-S transition. Recently, Che-1 was found to play an important role in the DNA damage response and cell-cycle checkpoint control. Genetic studies in mice revealed that Che-1 is essential for preimplantation development and the establishment of embryonic gene expression. Importantly, several findings showed that Che-1 participates in inhibiting apoptotic process. Thus, Che-1 emerges as an important adaptor that connects transcriptional regulation, cell-cycle progression, checkpoint control, and apoptosis.

Yoshida H (2003) Cell Struct Funct "The role of Apaf-1 in programmed cell death: from worm to tumor."

Yoshida H

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Cell Struct Funct,

2003]

Apoptosis or programmed cell death is an important process to eliminate unnecessary or hazardous cells. Apaf-1, a mammalian homologue of CED-4 of C. elegans, is the essential adaptor molecule in the mitochondrial pathway of apoptosis. Mice lacking Apaf-1 show accumulation of neurons in the developing central nervous system due to reduced apoptosis. Apaf-1-deficient cells are remarkably resistant to various apoptotic stimuli. Apaf-1-mediated apoptosis plays a role in the prevention of tumorigenesis. However, Apaf-1-independent cell death pathways are also indicated. In this review, we will summarize what has been learned about the role of Apaf-1 by biochemical and genetical approaches.

Topf U et al. (2019) Front Neurosci "Ancient Function of Teneurins in Tissue Organization and Neuronal Guidance in the Nematode Caenorhabditis elegans."

Topf U, Drabikowski K

[

Front Neurosci,

2019]

The nematode Caenorhabditis elegans expresses the ten-1 gene that encodes teneurin. TEN-1 protein is expressed throughout the life of C. elegans. The loss of ten-1 function results in embryonic and larval lethality, highlighting its importance for fundamental processes during development. TEN-1 is expressed in the epidermis and neurons. Defects in neuronal pathfinding and epidermal closure are characteristic of ten-1 loss-of-function mutations. The molecular mechanisms of TEN-1 function in neurite outgrowth, neuronal pathfinding, and dendritic morphology in C. elegans are largely unknown. Its genetic redundancy with the extracellular matrix receptors integrin and dystroglycan and genetic interactions with several basement membrane components suggest a role for TEN-1 in the maintenance of basement membrane integrity, which is essential for neuronal guidance. Identification of the lat-1 gene in C. elegans, which encodes latrophilin, as an interaction partner of ten-1 provides further mechanistic insights into TEN-1 function in neuronal development. However, receptor-ligand interactions between LAT-1 and TEN-1 remain to be experimentally proven. The present review discusses the function of teneurin in C. elegans, with a focus on its involvement in the formation of receptor signaling complexes and neuronal networks.

Semenza GL (2001) Cell "HIF-1, O(2), and the 3 PHDs: how animal cells signal hypoxia to the nucleus."

Semenza GL

[

Cell,

2001]

Hypoxia-inducible factor 1 (HIF-1) is a global regulator of cellular and systemic O2 homeostasis in animals. A molecular basis for O2 regulated expression of the HIF-1 alpha subunit has now been determined, providing a mechanism for changes in gene expression in response to changes in cellular oxygenation.

McGhee JD (2013) Wiley Interdiscip Rev Dev Biol "The Caenorhabditis elegans intestine."

McGhee JD

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Wiley Interdiscip Rev Dev Biol,

2013]

The transcriptional regulatory hierarchy that controls development of the Caenorhabditis elegans endoderm begins with the maternally provided SKN-1 transcription factor, which determines the fate of the EMS blastomere of the four-cell embryo. EMS divides to produce the posterior E blastomere (the clonal progenitor of the intestine) and the anterior MS blastomere, a major contributor to mesoderm. This segregation of lineage fates is controlled by an intercellular signal from the neighboring P2 blastomere and centers on the HMG protein POP-1. POP-1 would normally repress the endoderm program in both E and MS but two consequences of the P2-to-EMS signal are that POP-1 is exported from the E-cell nucleus and the remaining POP-1 is converted to an endoderm activator by complexing with SYS-1, a highly diverged -catenin. In the single E cell, a pair of genes encoding small redundant GATA-type transcription factors, END-1 and END-3, are transcribed under the combined control of SKN-1, the POP-1/SYS-1 complex, as well as the redundant pair of MED-1/2 GATA factors, themselves direct zygotic targets of SKN-1 in the EMS cell. With the expression of END-1/END-3, the endoderm is specified. END-1 and END-3 then activate transcription of a further set of GATA-type transcription factors that drive intestine differentiation and function. One of these factors, ELT-2, appears predominant; a second factor, ELT-7, is partially redundant with ELT-2. The mature intestine expresses several thousand genes, apparently all controlled, at least in part, by cis-acting GATA-type motifs.

Carter CS et al. (2002) Trends Genet "A critical analysis of the role of growth hormone and IGF-1 in aging and lifespan."

Carter CS, Sonntag WE, Ramsey MM

[

Trends Genet,

2002]

Studies in Caenorhabditis elegans demonstrate that disruption of the daf-2 signaling pathways extends lifespan. Similarities among the daf-2 pathway, insulin-like signaling in flies and yeast, and the mammalian insulin-like growth factor 1 (IGF-1) signaling cascade raise the possibility that modifications to IGF-1 signaling could also extend lifespan in mammals. In fact, growth hormone (GH)/IGF-1-deficient dwarf mice do live significantly longer than their wild-type counterparts. However, multiple endocrine deficiencies and developmental anomalies inherent in these models confound this interpretation. Here, we critique the current mammalian models of GH/IGF-1 deficiency and discuss the actions of GH/IGF-1 on biological aging and lifespan.

Curtis D (1994) Bioessays "Translational repression as a conserved mechanism for the regulation of embryonic polarity."

Curtis D

[

Bioessays,

1994]

The mechanisms used to establish embryonic polarity are still largely unknown. A recent paper((1)) describes the expression pattern of the gene glp-1, which is required for induction events during development of the nematode Caenorhabditis elegans. Although glg-1 RNA is found throughout the early embryo, Glp-1 protein is only expressed in anterior cells. This negative translational regulation in posterior cells is shown to be mediated through sequences in the glp-1 3'untranslated region (3'UTR). Thus in nematodes, as in Drosophila, translational repression is one mechanism used to establish the embryonic anterior-posterior axis.

Leiser SF et al. (2010) Biol Chem "The hypoxia-inducible factor HIF-1 functions as both a positive and negative modulator of aging."

Kaeberlein M, Leiser SF

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Biol Chem,

2010]

In the past year and a half, five studies have independently established a direct connection between the hypoxic response transcription factor, HIF-1, and aging in Caenorhabditis elegans. These studies demonstrated that HIF-1 can both promote and limit longevity via pathways that are mechanistically distinct. Here, we review the current state of knowledge regarding modulation of aging by HIF-1 and speculate on potential aspects of HIF-1 function that could be relevant for mammalian longevity and healthspan.

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