Hectd1 is essential for embryogenesis in mice.
Journal article

Hectd1 is essential for embryogenesis in mice.

  • D'Alonzo D Department of Biomedicine, University Hospital, University of Basel, Hebelstrasse 20, CH-4031, Basel, Switzerland.
  • Emch FH Clinic of Gynecological Endocrinology and Reproductive Medicine, University Hospital, University of Basel, Spitalstrasse 21, CH-4031, Basel, Switzerland.
  • Shen X Clinic of Gynecological Endocrinology and Reproductive Medicine, University Hospital, University of Basel, Spitalstrasse 21, CH-4031, Basel, Switzerland; Chongqing Reproductive and Genetics Institute, 64 Jing Tang ST, Yu Zhong District, Chongqing, 400013, PR China.
  • Bruder E Institute of Pathology, University Hospital, University of Basel, Schönbeinstrasse 40, CH-4031, Basel, Switzerland.
  • De Geyter C Department of Biomedicine, University Hospital, University of Basel, Hebelstrasse 20, CH-4031, Basel, Switzerland; Clinic of Gynecological Endocrinology and Reproductive Medicine, University Hospital, University of Basel, Spitalstrasse 21, CH-4031, Basel, Switzerland.
  • Zhang H Department of Biomedicine, University Hospital, University of Basel, Hebelstrasse 20, CH-4031, Basel, Switzerland. Electronic address: hong.zhang@usb.ch.
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  • 2019-07-14
Published in:
  • Gene expression patterns : GEP. - 2019
English Many aspects of the functional role of the E3 ubiquitin ligase Hectd1 in embryogenesis and in cell biology still remain to be elucidated. In order to contribute to this task we now report the generation of a new transgenic mouse model for Hectd1 using the gene trap strategy. The HECT domain deletion mutant mouse was created by inserting a β-geo cassette into the Hectd1 locus. Mice homozygous for Hectd1-mutant showed early embryonic lethality with abnormal placental development and defective of neural tube closure resulting in exencephaly. The thickness of the placenta of both Hectd1-mutant homozygous and heterozygous mice was distinctly thinner than that of wildtype mice, the difference being most pronounced in the labyrinth layer of the placenta. We also addressed the temporal and spatial expression profiles of Hectd1 in adult tissues by X-gal staining. Hectd1 expression was detected in specific cell populations of most but not all tissues of the adult organism. Furthermore, the expression of Hectd1 was regulated by insulin and by both heat and hypoxia. Thus, our studies reveal that Hectd1 is indispensable for normal embryogenesis and fetal survival. The generation of this new Hectd1 mutant mouse model provides ample opportunities to study the function of Hectd1 in mammalian cells in detail.
Language
  • English
Open access status
closed
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Persistent URL
https://folia.unifr.ch/global/documents/102131
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