CACN-1/Cactin interacts genetically with MIG-2 GTPase signaling to control distal tip cell migration in C. elegans

Tannoury, Hiba; Rodriguez, Varenka; Kovacevic, Ismar; Ibourk, Mouna; Lee, Myeongwoo; Cram, Erin J.

doi:10.1016/j.ydbio.2010.02.025

Cited by 35 publications

(49 citation statements)

References 41 publications

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“…It has been reported that [31][32][33]28]. Human Cactin has been reported to interact with IκBL, which is one of negative regulators of the NFκB signaling pathway [27].…”

Section: Discussionmentioning

confidence: 99%

TRIM39 negatively regulates the NFκB-mediated signaling pathway through stabilization of Cactin

Suzuki

Watanabe

Nakamaru

et al. 2015

Cell. Mol. Life Sci.

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NFκB is one of the central regulators of cell survival, immunity, inflammation, carcinogenesis and organogenesis. The activation of NFκB is strictly regulated by several posttranslational modifications including phosphorylation, neddylation and ubiquitination. Several types of ubiquitination play important roles in multi-step regulations of the NFκB pathway. Some of the tripartite motif-containing (TRIM) proteins functioning as E3 ubiquitin ligases are known to regulate various biological processes such as inflammatory signaling pathways. One of the TRIM family proteins, TRIM39, for which the gene has single nucleotide polymorphisms (SNPs), has been identified as one of the genetic factors in Behcet's disease. However, the role of TRIM39 in inflammatory signaling had not been fully elucidated. In this study, to elucidate the function of TRIM39 in inflammatory signaling, we performed yeast two-hybrid screening using TRIM39 as a bait and identified Cactin, which has been reported to inhibit NFκB and TLR-mediated transcriptions. We show that TRIM39 stabilizes Cactin protein and that Cactin is upregulated after TNFα stimulation. TRIM39 knockdown also causes activation of the NFκB signal.These findings suggest that TRIM39 negatively regulates the NFκB signal in collaboration with Cactin induced by inflammatory stimulants such as TNFα.

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“…It has been reported that [31][32][33]28]. Human Cactin has been reported to interact with IκBL, which is one of negative regulators of the NFκB signaling pathway [27].…”

Section: Discussionmentioning

confidence: 99%

TRIM39 negatively regulates the NFκB-mediated signaling pathway through stabilization of Cactin

Suzuki

Watanabe

Nakamaru

et al. 2015

Cell. Mol. Life Sci.

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“…Human cactin was later found to physically and functionally interact with IκB-like protein (IκBL) and to be part of a negative feedback loop that controls NFκB transcriptional response (Suzuki et al, 2016), suggesting a conserved function for cactins in immune response and development (Atzei et al, 2010a). To date, cactin orthologs have been studied also in Toxoplasma gondii, Litopenaeus vannamei, Arabidopsis thaliana, Caenorhabditis elegans, and Danio rerio (Atzei et al, 2010b;Baldwin et al, 2013;Cecchetelli et al, 2016;Doherty et al, 2014;LaBonty et al, 2014;Szatanek et al, 2012;Tannoury et al, 2010;Zhang et al, 2014). In these organisms, cactin loss-of-function is associated with compromised cell viability and proliferation, and with developmental defects, highlighting the essentiality of cactin proteins.…”

Section: Introductionmentioning

confidence: 99%

Human cactin interacts with DHX8 and SRRM2 to assure efficient pre-mRNA splicing and sister chromatid cohesion

Zanini

Soneson

Lorenzi

et al. 2017

Journal of Cell Science

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Cactins constitute a family of eukaryotic proteins broadly conserved from yeast to human and required for fundamental processes such as cell proliferation, genome stability maintenance, organismal development and immune response. Cactin proteins have been found to associate with the spliceosome in several model organisms, nevertheless their molecular functions await elucidation. Here we show that depletion of human cactin leads to premature sister chromatid separation, genome instability and cell proliferation arrest. Moreover, cactin is essential for efficient splicing of thousands of pre-mRNAs, and incomplete splicing of the pre-mRNA of sororin (also known as CDCA5), a cohesin-associated factor, is largely responsible for the aberrant chromatid separation in cactin-depleted cells. Lastly, cactin physically and functionally interacts with the spliceosome-associated factors DHX8 and SRRM2. We propose that cellular complexes comprising cactin, DHX8 and SRRM2 sustain precise chromosome segregation, genome stability and cell proliferation by allowing faithful splicing of specific pre-mRNAs. Our data point to novel pathways of gene expression regulation dependent on cactin, and provide an explanation for the pleiotropic dysfunctions deriving from cactin inactivation in distant eukaryotes.

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“…For example, CCDC-55, a coiled-coil containing protein of unknown function found in an operon with rnf-121 and rnf-5 , two E3 ubiquitin ligases, CACN-1, another coiled-coiled containing protein, homologous to the IKB/cactus binding protein CACTIN, and MIG-39, a nuclear BED finger domain protein have all been found to be necessary for proper cessation of DTC migration (9, 63–65). Depletion of these genes via RNAi or by mutation results in gonad arms that migrate far past the vulva on the dorsal surface (Figure 4B).…”

Section: The Dtc Stops Migrating At a Specific Place And Timementioning

confidence: 99%

“…Often, the DTCs only stop migrating when unable to squeeze past the pharynx, or upon reaching the posterior end of the animal (65). Although the mechanism is not fully understood, CACN-1 and its homologs are emerging as regulators of splicing and/or post-transcriptional gene expression.…”

Section: The Dtc Stops Migrating At a Specific Place And Timementioning

confidence: 99%

Regulating distal tip cell migration in space and time

Cecchetelli

Cram

2017

Mechanisms of Development

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Gonad morphogenesis in the nematode C. elegans is guided by two leader cells, the distal tip cells (DTC). The DTCs migrate along a stereotyped path, executing two 90° turns before stopping at the midpoint of the animal. This migratory path determines the double-U shape of the adult gonad, therefore, the path taken by the DTCs can be inferred from the final shape of the organ. In this review, we focus on the mechanism by which the DTC executes the first 90° turn from the ventral to dorsal side of the animal, and how it finds its correct stopping place at the midpoint of the animal. We discuss the role of heterochronic genes in coordinating DTC migration with larval development, the role of feedback loops and miRNA regulation in phenotypic robustness, and the role of RNA binding proteins in the cessation of DTC migration.

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CACN-1/Cactin interacts genetically with MIG-2 GTPase signaling to control distal tip cell migration in C. elegans

Cited by 35 publications

References 41 publications

TRIM39 negatively regulates the NFκB-mediated signaling pathway through stabilization of Cactin

TRIM39 negatively regulates the NFκB-mediated signaling pathway through stabilization of Cactin

Human cactin interacts with DHX8 and SRRM2 to assure efficient pre-mRNA splicing and sister chromatid cohesion

Regulating distal tip cell migration in space and time

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