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Egfl6 is involved in zebrafish notochord development.

Xueqian Wang1, Xin Wang, Wei Yuan

  • 1Co-innovation Center of Neuroregeneration, Jiangsu Key Laboratory of Neuroregeneration, Nantong University, Qixiu Road 19, 226001, Nantong, China.

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Epidermal growth factor-like 6 (Egfl6) is crucial for zebrafish notochord development. Inhibiting Notch signaling rescues Egfl6 deficiency, highlighting its role in vertebrate embryonic development.

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Area of Science:

  • Developmental biology
  • Molecular biology
  • Genetics

Background:

  • The epidermal growth factor (EGF) repeat motif is found in proteins regulating diverse cellular processes.
  • Egfl6 (Epidermal Growth Factor-Like 6), also known as MAGE, is an EGF protein with limited in vivo functional studies in vertebrates.
  • Previous research has not fully elucidated the expression patterns and functions of Egfl6 during vertebrate embryonic development.

Purpose of the Study:

  • To investigate the expression pattern of Egfl6 in zebrafish embryos.
  • To analyze the functional role of Egfl6 in zebrafish embryonic development, particularly in notochord formation.
  • To explore the relationship between Egfl6 and Notch signaling in notochord development.

Main Methods:

  • Zebrafish model system for in vivo studies.
  • Whole-mount in situ hybridization to determine mRNA expression patterns.
  • Morpholino-induced knockdown of Egfl6 to assess functional consequences.
  • Pharmacological inhibition of Notch signaling using DAPT.

Main Results:

  • Egfl6 mRNA expression was detected in somites, fin epidermis, pharyngeal arches, and hindbrain.
  • Secreted Egfl6 protein accumulated significantly in the notochord.
  • Loss of Egfl6 function led to curved bodies and distorted notochords in zebrafish embryos.
  • Notch2 expression was upregulated in Egfl6 morphants, while other Notch components remained unaffected.
  • DAPT treatment rescued notochord developmental defects in Egfl6-deficient embryos.

Conclusions:

  • Egfl6 plays a significant role in zebrafish notochord development.
  • Egfl6 deficiency causes notochord malformations, indicating its importance in axial skeleton formation.
  • Notch signaling, specifically Notch2, is involved in the developmental pathway affected by Egfl6 deficiency.
  • Inhibition of Notch signaling can rescue Egfl6-related notochord defects, suggesting a therapeutic target for related developmental disorders.