Trim36/Haprin plays a critical role in the arrangement of somites during Xenopus embryogenesis

Yoshigai, Emi; Kawamura, Shinobu; Kuhara, Satoru; Tashiro, Kosuke

doi:10.1016/j.bbrc.2008.11.069

Cited by 23 publications

(14 citation statements)

References 22 publications

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“…Although we did not specifically address germ-cell formation in this study, it is possible that Trim36 also functions in specifying primordial germ cells. Targeted interference with Trim36 function in germ-plasm-containing cells could address these questions, although morpholino inhibition of zygotic Trim36 function disrupts morphogenesis and somite arrangement (Yoshigai et al, 2009), making the study of primordial germ cells problematic.…”

Section: Discussionmentioning

confidence: 99%

Vegetally localized Xenopus trim36 regulates cortical rotation and dorsal axis formation

Cuykendall

Houston

2009

Development

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Specification of the dorsoventral axis in Xenopus depends on rearrangements of the egg vegetal cortex following fertilization, concomitant with activation of Wnt/β-catenin signaling. How these processes are tied together is not clear, but RNAs localized to the vegetal cortex during oogenesis are known to be essential. Despite their importance, few vegetally localized RNAs have been examined in detail. In this study, we describe the identification of a novel localized mRNA, trim36, and characterize its function through maternal loss-of-function experiments. We find that trim36 is expressed in the germ plasm and encodes a ubiquitin ligase of the Tripartite motif-containing (Trim) family. Depletion of maternal trim36 using antisense oligonucleotides results in ventralized embryos and reduced organizer gene expression. We show that injection of wnt11 mRNA rescues this effect, suggesting that Trim36 functions upstream of Wnt/β-catenin activation. We further find that vegetal microtubule polymerization and cortical rotation are disrupted in trim36-depleted embryos, in a manner dependent on Trim36 ubiquitin ligase activity. Additionally, these embryos can be rescued by tipping the eggs 90° relative to the animal-vegetal axis. Taken together, our results suggest a role for Trim36 in controlling the stability of proteins regulating microtubule polymerization during cortical rotation, and subsequently axis formation.

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Section: Discussionmentioning

confidence: 99%

Vegetally localized Xenopus trim36 regulates cortical rotation and dorsal axis formation

Cuykendall

Houston

2009

Development

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“…The TRIM36 protein is a multidomain E3 ubiquitin ligase that interacts with centromere protein-H and may be involved in differentiation and development during embryogenesis [ 54 , 55 ]. This protein may be involved in protein–protein interactions [ 56 ], with a function in cell adhesion [ 57 ], the process implicated in the pathogenesis of ADHD by several previous studies [ 16 , 17 , 21 , 58 ].…”

Section: Discussionmentioning

confidence: 99%

Genome-Wide Analysis of Attention Deficit Hyperactivity Disorder in Norway

et al. 2015

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BackgroundAttention deficit hyperactivity disorder (ADHD) is a highly heritable neuropsychiatric condition, but it has been difficult to identify genes underlying this disorder. This study aimed to explore genetics of ADHD in an ethnically homogeneous Norwegian population by means of a genome-wide association (GWA) analysis followed by examination of candidate loci.Materials and MethodsParticipants were recruited through Norwegian medical and birth registries as well as the general population. Presence of ADHD was defined according to DSM-IV criteria. Genotyping was performed using Illumina Human OmniExpress-12v1 microarrays. Statistical analyses were divided into several steps: (1) genome-wide association in the form of logistic regression in PLINK and follow-up pathway analyses performed in DAPPLE and INRICH softwares, (2) SNP-heritability calculated using genome-wide complex trait analysis (GCTA) tool, (3) gene-based association tests carried out in JAG software, and (4) evaluation of previously reported genome-wide signals and candidate genes of ADHD.ResultsIn total, 1.358 individuals (478 cases and 880 controls) and 598.384 autosomal SNPs were subjected to GWA analysis. No single polymorphism reached genome-wide significance. The strongest signal was observed at rs9949006 in the ENSG00000263745 gene (OR=1.51, 95% CI 1.28–1.79, p=1.38E-06). Pathway analyses of the top SNPs implicated genes involved in the regulation of gene expression, cell adhesion and inflammation. Among previously identified ADHD candidate genes, prominent association signals were observed for SLC9A9 (rs1393072, OR=1.46, 95% CI = 1.21–1.77, p=9.95E-05) and TPH2 (rs17110690, OR = 1.38, 95% CI = 1.14–1.66, p=8.31E-04).ConclusionThis study confirms the complexity and heterogeneity of ADHD etiology. Taken together with previous findings, our results point to a spectrum of biological mechanisms underlying the symptoms of ADHD, providing targets for further genetic exploration of this complex disorder.

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“…In Xenopus laevis, TRIM33/Ectodermin is essential for the specification of the ectoderm germ layer and acts by restricting the mesoderm-inducing activity of TGF signals to the mesoderm and favoring neural induction (Dupont et al, 2005). TRIM36/Haprin mRNA is instead enriched in the vegetal cortex of Xenopus oocytes and required for cortical rotation, dorsal axis determination and somite arrangement (Cuykendall and Houston, 2009;Yoshigai et al, 2009). In chick and rat, both TRIM32 and TRIM54/Murf1 expression is induced during myogenic differentiation and impairing of their function has been linked with forms of muscular dystrophy (Bodine et al, 2001;Kudryashova et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Specific expression of a TRIM-containing factor in ectoderm cells affects the skeletal morphogenetic program of the sea urchin embryo

2011

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SUMMARYIn the indirect developing sea urchin embryo, the primary mesenchyme cells (PMCs) acquire most of the positional and temporal information from the overlying ectoderm for skeletal initiation and growth. In this study, we characterize the function of the novel gene strim1, which encodes a tripartite motif-containing (TRIM) protein, that adds to the list of genes constituting the epithelial-mesenchymal signaling network. We report that strim1 is expressed in ectoderm regions adjacent to the bilateral clusters of PMCs and that its misexpression leads to severe skeletal abnormalities. Reciprocally, knock down of strim1 function abrogates PMC positioning and blocks skeletogenesis. Blastomere transplantation experiments establish that the defects in PMC patterning, number and skeletal growth depend upon strim1 misexpression in ectoderm cells. Furthermore, clonal expression of strim1 into knocked down embryos locally restores skeletogenesis. We also provide evidence that the Otp and Pax2/5/8 regulators, as well as FGFA, but not VEGF, ligand act downstream to strim1 in ectoderm cells, and that strim1 triggers the expression of the PMC marker sm30, an ectoderm-signaling dependent gene. We conclude that the strim1 function elicits specific gene expression both in ectoderm cells and PMCs to guide the skeletal biomineralization during morphogenesis.

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Trim36/Haprin plays a critical role in the arrangement of somites during Xenopus embryogenesis

Cited by 23 publications

References 22 publications

Vegetally localized Xenopus trim36 regulates cortical rotation and dorsal axis formation

Vegetally localized Xenopus trim36 regulates cortical rotation and dorsal axis formation

Genome-Wide Analysis of Attention Deficit Hyperactivity Disorder in Norway

Specific expression of a TRIM-containing factor in ectoderm cells affects the skeletal morphogenetic program of the sea urchin embryo

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