Goosecoid suppresses cell growth and enhances neuronal differentiation of PC12 cells

Sawada, Ken; Konishi, Yuko; Tominaga, Mari; Watanabe, Yuji; Hirano, Jun; Inoue, Shimpei; Kageyama, Ryoichiro; Blum, Martin; Tominaga, Akira

doi:10.1242/jcs.113.15.2705

Cited by 9 publications

(1 citation statement)

References 41 publications

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“…In addition, in our study, GSC , SORBS1 and NDRG2 mRNA were down-expressed in Sotos patients compared to the healthy controls. These three genes encode proteins that are associated with the actin cytoskeleton, the formation of actin stress fibers and focal adhesions, and receptor tyrosinase kinase-signaling, and they control different aspects of morphogenesis and cell differentiation [ 53 , 54 , 55 ]. Some studies have reported that the expression of GSC inhibits the proliferation of PC12 cells and that—as with NSD1—GSC mediates the regulation of erythropoiesis functions [ 56 ].…”

Section: Discussionmentioning

confidence: 99%

NSD1 Mutations in Sotos Syndrome Induce Differential Expression of Long Noncoding RNAs, miR646 and Genes Controlling the G2/M Checkpoint

Conteduca

Cangelosi

Coco

et al. 2022

Life

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An increasing amount of evidence indicates the critical role of the NSD1 gene in Sotos syndrome (SoS), a rare genetic disease, and in tumors. Molecular mechanisms affected by NSD1 mutations are largely uncharacterized. In order to assess the impact of NSD1 haploinsufficiency in the pathogenesis of SoS, we analyzed the gene expression profile of fibroblasts isolated from the skin samples of 15 SoS patients and of 5 healthy parents. We identified seven differentially expressed genes and five differentially expressed noncoding RNAs. The most upregulated mRNA was stratifin (SFN) (fold change, 3.9, Benjamini–Hochberg corrected p < 0.05), and the most downregulated mRNA was goosecoid homeobox (GSC) (fold change, 3.9, Benjamini–Hochberg corrected p < 0.05). The most upregulated lncRNA was lnc-C2orf84-1 (fold change, 4.28, Benjamini–Hochberg corrected p < 0.001), and the most downregulated lncRNA was Inc-C15orf57 (fold change, −0.7, Benjamini–Hochberg corrected p < 0.05). A gene set enrichment analysis reported the enrichment of genes involved in the KRAS and E2F signaling pathways, splicing regulation and cell cycle G2/M checkpoints. Our results suggest that NSD1 is involved in cell cycle regulation and that its mutation can induce the down-expression of genes involved in tumoral and neoplastic differentiation. The results contribute to defining the role of NSD1 in fibroblasts for the prevention, diagnosis and control of SoS.

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Section: Discussionmentioning

confidence: 99%

NSD1 Mutations in Sotos Syndrome Induce Differential Expression of Long Noncoding RNAs, miR646 and Genes Controlling the G2/M Checkpoint

Conteduca

Cangelosi

Coco

et al. 2022

Life

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Quantification of NGF-dependent neuronal differentiation of PC-12 cells by means of neurofilament-L mRNA expression and neuronal outgrowth

Schimmelpfeng¹,

Weibezahn²,

Dertinger³

2004

Journal of Neuroscience Methods

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A cell cycle arrest is necessary for bottle cell formation in the early Xenopus gastrula: Integrating cell shape change, local mitotic control and mesodermal patterning

Kurth

2005

Mechanisms of Development

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During development cell proliferation and morphogenetic movements are tightly intermingled. Both processes depend on the same cytoskeletal elements. Therefore, precise regulation of local mitotic activity seems to be basic for proper embryogenesis. Here, I report on bottle cells as an early non-mitotic cell population in the Xenopus gastrula. Endogenous and activin/BVg1-induced ectopic bottle cells do not proliferate. Overexpression of the mitosis-promoting phosphatase cdc25C increases the proliferation rate and interferes with bottle cell formation whereas the phosphatase-dead mutant cdc25C(C457A) does not. Cdc25C also affects other gastrulation processes such as epiboly, vegetal rotation or tissue separation as inferred from histological inspection of early gastrulae. Double stainings of gsc/Xbra transcripts and mitotic nuclei in ectopic and endogenous lips demonstrated that non-mitotic cells occur in the bottle cell region and, to a lesser extent, in the gsc domain which both are indicative of high TGF-beta signalling. In contrast, the Xbra-region and the remainder of the animal cap appear to be permissive for higher rates of cell proliferation. These data suggest inhibition of cell proliferation by high levels of activin-type signals and a close link of mesodermal and mitotic patterning. Finally, coexpression of eFGF together with activin/BVg1 interferes with TGF-beta-induced bottle cell formation. This inhibitory effect correlates with increased cell proliferation as compared to embryos injected with activin/BVg1 alone. Taken together, these data suggest that TGF-beta and FGF signals play antagonistic roles in bottle cell formation and the spatial control of the cell cycle in early Xenopus gastrulae.

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Goosecoid suppresses cell growth and enhances neuronal differentiation of PC12 cells

Cited by 9 publications

References 41 publications

NSD1 Mutations in Sotos Syndrome Induce Differential Expression of Long Noncoding RNAs, miR646 and Genes Controlling the G2/M Checkpoint

NSD1 Mutations in Sotos Syndrome Induce Differential Expression of Long Noncoding RNAs, miR646 and Genes Controlling the G2/M Checkpoint

Quantification of NGF-dependent neuronal differentiation of PC-12 cells by means of neurofilament-L mRNA expression and neuronal outgrowth

A cell cycle arrest is necessary for bottle cell formation in the early Xenopus gastrula: Integrating cell shape change, local mitotic control and mesodermal patterning

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