CUTI-1: A Novel Tetraspan Protein Involved in C. elegans CUTicle Formation and Epithelial Integrity

Fritz, Julie-Anne; Behm, Carolyn A.

doi:10.1371/journal.pone.0005117

Cited by 19 publications

(14 citation statements)

References 36 publications

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“…As lethality coincides with the molt, mcm-4 mutants might die from reduced integrity of the cuticle. Expression of mcm-4 in the epidermis of mcm-4 mutants prevents the loss of seam cells that normally contribute to cuticle formation (Figs S6B; (see Fritz and Behm, 2009 and references therein). Moreover, mcm-4 expression in the syncytial epidermis restores endoreduplication, which may promote growth as well as cuticle secretion.…”

Section: Discussionmentioning

confidence: 99%

C. elegans MCM-4 is a general DNA replication and checkpoint component with an epidermis-specific requirement for growth and viability

Korzelius

Ruijtenberg

Portegijs

et al. 2011

Developmental Biology

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DNA replication and its connection to M phase restraint are studied extensively at the level of single cells but rarely in the context of a developing animal. C. elegans lin-6 mutants lack DNA synthesis in postembryonic somatic cell lineages, while entry into mitosis continues. These mutants grow slowly and either die during larval development or develop into sterile adults. We found that lin-6 corresponds to mcm-4 and encodes an evolutionarily conserved component of the MCM2-7 pre-RC and replicative helicase complex. The MCM-4 protein is expressed in all dividing cells during embryonic and postembryonic development and associates with chromatin in late anaphase. Induction of cell-cycle entry and differentiation continues in developing mcm-4 larvae, even in cells that went through abortive division. In contrast to somatic cells in mcm-4 mutants, the gonad continues DNA replication and cell division until late larval development. Expression of MCM-4 in the epidermis (also known as hypodermis) is sufficient to rescue the growth retardation and lethality of mcm-4 mutants. While the somatic gonad and germline show substantial ability to cope with lack of zygotic mcm-4 function, mcm-4 is specifically required in the epidermis for growth and survival of the whole organism. Thus, C. elegans mcm-4 has conserved functions in DNA replication and replication checkpoint control but also shows unexpected tissue-specific requirements.

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Section: Discussionmentioning

confidence: 99%

C. elegans MCM-4 is a general DNA replication and checkpoint component with an epidermis-specific requirement for growth and viability

Korzelius

Ruijtenberg

Portegijs

et al. 2011

Developmental Biology

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“…The pLenti CMV GFP Puro plasmid was a gift from Eric Campeau (Addgene #17448) [14]. Pool of GFP positive cells were then sorted with fluorescence activated cell sorting using Sony SH800Z Cell Sorter.…”

Section: Methodsmentioning

confidence: 99%

Motility of glioblastoma cells is driven by netrin-1 induced gain of stemness

Ylivinkka

Sihto

Tynninen

et al. 2017

J Exp Clin Cancer Res

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BackgroundGlioblastoma is an untreatable brain cancer. The tumors contain a population of stem-like cells which are highly invasive and resistant to therapies. These cells are the main reason for the lethality of glioblastoma. Extracellular guidance molecule netrin-1 promotes the invasiveness and survival of various cancer cell types. We have previously found that netrin-1 activates Notch signaling, and Notch signaling associates with cell stemness. Therefore, we have here investigated the effects of netrin-1 on glioblastoma pathogenesis and glioblastoma cell stemness.MethodsGlioma tissue microarrays were stained with immunohistochemistry and the results were used to evaluate the association between netrin-1 and survival of glioma patients. The localization of netrin-1 was analyzed utilizing fresh frozen glioblastoma tissues. The glioma cell invasion was investigated using ex vivo glioma tissue cultures and newly established primary cell cultures in 3D in vitro invasion assays. Intracranial mouse xenograft models were utilized to investigate the effects of netrin-1 on glioblastoma growth and invasion in vivo.ResultsNetrin-1 expression associated with poor patient prognosis in grade II-III gliomas. In addition, its expression correlated with the stem-like cell marker nestin. Netrin-1 overexpression in cultured cells led to increased formation of stem-like cell spheroids. In glioblastoma tumor biopsies netrin-1 localized to hypoxic tumor areas known to be rich in the stem-like cells. In xenograft mouse models netrin-1 expression altered the phenotype of non-invasive glioblastoma cells into diffusively invading and increased the expression of glioma stem-like cell markers. Furthermore, a distinct invasion pattern where netrin-1 positive cells were following the invasive stem-like cells was detected both in mouse models and ex vivo human glioblastoma tissue cultures. Inhibition of netrin-1 signaling targeted especially the stem-like cells and inhibited their infiltrative growth.ConclusionsOur findings describe netrin-1 as an important regulator of glioblastoma cell stemness and motility. Netrin-1 activates Notch signaling in glioblastoma cells resulting in subsequent gain of stemness and enhanced invasiveness of these cells. Moreover, inhibition of netrin-1 signaling may offer a way to target stem-like cells.Electronic supplementary materialThe online version of this article (doi:10.1186/s13046-016-0482-0) contains supplementary material, which is available to authorized users.

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“…3E and F). The adult alae are parts of the cuticle structure secreted by seam cells, which are lateral hypodermal cells (14,19). The seam cells go through several divisions during each larval stage.…”

Section: Downregulation Of Pod-2 or Fasn-1 Causes Disruption Of The Cmentioning

confidence: 99%

“…The C. elegans molting process involves a coordinated interplay between proteases [e.g., NAS-37 (3,4)] and other proteins. These include cholesterol transport proteins (5), transcription factors [e.g., NHR-23 (6)(7)(8)], extracellular transport proteins, transmembrane proteins, and extracellular matrix (ECM) enzymes (9)(10)(11)(12)(13)(14). Because this process involves extensive tissue remodeling entailing degradation of old cuticle proteins, inactivation of these proteases during the ecdysis step can cause molting defects in C. elegans (4).…”

Section: Introductionmentioning

confidence: 99%

A potential role for fatty acid biosynthesis genes during molting and cuticle formation in Caenorhabditis elegans

Li¹,

Paik²

2011

BMB Reports

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Caenorhabditis elegans undergoes a developmental molting process that involves a coordinated interplay among diverse intracellular pathways. Here, we investigated the functions of two fatty acid biosynthesis genes; pod-2, encoding acetyl-CoA carboxylase, and fasn-1, encoding fatty acid synthase, in the C. elegans molting process. Although both the pod-2 and fasn-1 genes were expressed at constant levels throughout C. elegans development, knockdown of the proteins encoded by these genes using RNA interference produced severe defects in triglyceride production, molting, and reproduction that were coupled to suppression of NAS-37, a metalloprotease. An assessment of the structure and integrity of the cuticle using a COL-19::GFP marker and Hoechst 33258 staining showed that downregulation of either pod-2 or fasn-1 impaired cuticle formation and disrupted the integrity of the cuticle and the hypodermal membrane. [BMB reports 2011; 44(4): 285-290]

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CUTI-1: A Novel Tetraspan Protein Involved in C. elegans CUTicle Formation and Epithelial Integrity

Cited by 19 publications

References 36 publications

C. elegans MCM-4 is a general DNA replication and checkpoint component with an epidermis-specific requirement for growth and viability

C. elegans MCM-4 is a general DNA replication and checkpoint component with an epidermis-specific requirement for growth and viability

Motility of glioblastoma cells is driven by netrin-1 induced gain of stemness

A potential role for fatty acid biosynthesis genes during molting and cuticle formation in Caenorhabditis elegans

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