Changes in Activity of the Regulatory Glycolytic Enzymes and of the Pyruvate-Dehydrogenase Complex during the Development of &lt;i&gt;Xenopus laevis&lt;/i&gt;

Raddatz, Eric; Løvtrup-Rein, Huguette

doi:10.1159/000163344

Cited by 5 publications

(6 citation statements)

References 15 publications

(21 reference statements)

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“…Organ situs defects in pfkp morphants were dose-dependent (data not shown). Consistent with previous reports demonstrating PFK-1 expression in early development [35][36][37], pfkp was expressed throughout stages known to be important for L-R patterning in Xenopus (figure 2b). These results indicated that pfkp but not pitrm1 was a suitable candidate for further study.…”

Section: Results (A) Genetic Analyses Of Patients With Heterotaxy Idesupporting

confidence: 92%

“…Our study (figure 2b) and others [35][36][37] have shown that PFK-1 is expressed throughout early Xenopus development. Expression is most readily detected in the animal pole and marginal zone during gastrulation, and at high levels in the neural tube, neural crest and adjacent tissue during neurulation [64].…”

Section: (B) Copy Number Variant Analyses Identify Novel Heterotaxy Gsupporting

confidence: 72%

“…In Xenopus, catalytic activity of PFK-1 isoforms [35] and overall rates of glycolysis [36] are very low until gastrulation [36]. As L-R patterning mechanisms may operate during early cleavage stages [66], roles for PFKP in L-R patterning could manifest in the pre-gastrula.…”

Section: (B) Copy Number Variant Analyses Identify Novel Heterotaxy Gene Candidatesmentioning

confidence: 99%

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Copy number variation as a genetic basis for heterotaxy and heterotaxy-spectrum congenital heart defects

Cowan

Tariq

Shaw

et al. 2016

Phil. Trans. R. Soc. B

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Genomic disorders and rare copy number abnormalities are identified in 15–25% of patients with syndromic conditions, but their prevalence in individuals with isolated birth defects is less clear. A spectrum of congenital heart defects (CHDs) is seen in heterotaxy, a highly heritable and genetically heterogeneous multiple congenital anomaly syndrome resulting from failure to properly establish left–right (L-R) organ asymmetry during early embryonic development. To identify novel genetic causes of heterotaxy, we analysed copy number variants (CNVs) in 225 patients with heterotaxy and heterotaxy-spectrum CHDs using array-based genotyping methods. Clinically relevant CNVs were identified in approximately 20% of patients and encompassed both known and putative heterotaxy genes. Patients were carefully phenotyped, revealing a significant association of abdominal situs inversus with pathogenic or likely pathogenic CNVs, while d-transposition of the great arteries was more frequently associated with common CNVs. Identified cytogenetic abnormalities ranged from large unbalanced translocations to smaller, kilobase-scale CNVs, including a rare, single exon deletion in ZIC3, a gene known to cause X-linked heterotaxy. Morpholino loss-of-function experiments in Xenopus support a role for one of these novel candidates, the platelet isoform of phosphofructokinase-1 ( PFKP ) in heterotaxy. Collectively, our results confirm a high CNV yield for array-based testing in patients with heterotaxy, and support use of CNV analysis for identification of novel biological processes relevant to human laterality. This article is part of the themed issue ‘Provocative questions in left–right asymmetry’.

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Section: Results (A) Genetic Analyses Of Patients With Heterotaxy Idesupporting

confidence: 92%

Section: (B) Copy Number Variant Analyses Identify Novel Heterotaxy Gsupporting

confidence: 72%

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Copy number variation as a genetic basis for heterotaxy and heterotaxy-spectrum congenital heart defects

Cowan

Tariq

Shaw

et al. 2016

Phil. Trans. R. Soc. B

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“…Interestingly, variations in Hex activity during embryogenesis as we observed here (Figure 4F) have also been reported in the frog Xenopus laevis [54]. In Xenopus Hex activity could be rate-limiting at relatively late developmental stage before hatching.…”

Section: Discussionsupporting

confidence: 86%

Glycogen and Glucose Metabolism Are Essential for Early Embryonic Development of the Red Flour Beetle Tribolium castaneum

et al. 2013

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Control of energy metabolism is an essential process for life. In insects, egg formation (oogenesis) and embryogenesis is dependent on stored molecules deposited by the mother or transcribed later by the zygote. In oviparous insects the egg becomes an isolated system after egg laying with all energy conversion taking place during embryogenesis. Previous studies in a few vector species showed a strong correlation of key morphogenetic events and changes in glucose metabolism. Here, we investigate glycogen and glucose metabolism in the red flour beetle Tribolium castaneum, an insect amenable to functional genomic studies. To examine the role of the key enzymes on glycogen and glucose regulation we cloned and analyzed the function of glycogen synthase kinase 3 (GSK-3) and hexokinase (HexA) genes during T. castaneum embryogenesis. Expression analysis via in situ hybridization shows that both genes are expressed only in the embryonic tissue, suggesting that embryonic and extra-embryonic cells display different metabolic activities. dsRNA adult female injection (parental RNAi) of both genes lead a reduction in egg laying and to embryonic lethality. Morphological analysis via DAPI stainings indicates that early development is impaired in Tc-GSK-3 and Tc-HexA1 RNAi embryos. Importantly, glycogen levels are upregulated after Tc-GSK-3 RNAi and glucose levels are upregulated after Tc-HexA1 RNAi, indicating that both genes control metabolism during embryogenesis and oogenesis, respectively. Altogether our results show that T. castaneum embryogenesis depends on the proper control of glucose and glycogen.

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“…The sugar uptake ability of xGLUT1 was not analyzed here, however, xGLUT1 possesses the relevant amino acid motif (R-X-G-R-R) conserved among GLUT-family members that determines the membrane topology required for the sugar transport activity of GLUT1 (Sato and Mueckler, 1999). Classical experiments in amphibian showed that glycolysis starts before gastrulation begins and that glycogen distribution in the dorsal blastopore lip is higher than in the ventral regions at the late blastula and gastrula stages (Miranda, 1977;Raddatz and Lovtrup-Rein, 1986;Saxen and Toivonen, 1962). These findings suggest that energy for gastrulation movement is supplied by glycolysis, implying that xGLUT1 might be required for this glycolysis via its glucose uptake activity.…”

Section: Discussionmentioning

confidence: 99%

Xenopus glucose transporter 1 (xGLUT1) is required for gastrulation movement in Xenopus laevis

Suzawa¹,

Yukita²,

Hayata³

et al. 2007

Int. J. Dev. Biol.

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Glucose transporters (GLUTs) are transmembrane proteins that play an essential role in sugar uptake and energy supply. Thirteen GLUT genes have been described and GLUT1 is the most abundantly expressed member of the family in animal tissues. Deficiencies in human GLUT1 are associated with many diseases, such as metabolic abnormalities, congenital brain defects and oncogenesis. It was suggested recently that Xenopus GLUT1 (xGLUT1) is upregulated by Activin/ Nodal signaling, although the developmental role of xGLUT1 remains unclear. Here, we investigated the expression pattern and function of xGLUT1 during Xenopus development. Wholemount in situ hybridization analysis showed expression of xGLUT1 in the mesodermal region of Xenopus embryos, especially in the dorsal blastopore lip at the gastrula stage. From the neurula stage, it was expressed in the neural plate, eye field, cement gland and somites. Loss-of-function analyses using morpholino antisense oligonucleotides against xGLUT1 (xGLUT1MO) caused microcephaly and axis elongation error. This elongation defect of activin-treated animal caps occurred without downregulation of early mesodermal markers. Moreover, dorsal-marginal explant analysis revealed that cell movement was suppressed in dorsal marginal zones injected with xGLUT1MO. These findings implicate xGLUT1 as an important player during gastrulation cell movement in Xenopus.

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Changes in Activity of the Regulatory Glycolytic Enzymes and of the Pyruvate-Dehydrogenase Complex during the Development of <i>Xenopus laevis</i>

Cited by 5 publications

References 15 publications

Copy number variation as a genetic basis for heterotaxy and heterotaxy-spectrum congenital heart defects

Copy number variation as a genetic basis for heterotaxy and heterotaxy-spectrum congenital heart defects

Glycogen and Glucose Metabolism Are Essential for Early Embryonic Development of the Red Flour Beetle Tribolium castaneum

Xenopus glucose transporter 1 (xGLUT1) is required for gastrulation movement in Xenopus laevis

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