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Proper closure of the optic fissure requires ephrin A5-EphB2-JNK signaling

Hyuna Noh1, Haeryung Lee1, Eunjeong Park1

  • 1Department of Biological Science, Sookmyung Women's University, Chungpa-ro 47gil 100, Yongsan-gu, Seoul 140-742, Korea.

Development (Cambridge, England)
|February 4, 2016
PubMed

Insights

Reduced apoptosis in the eye's optic cup disrupts optic fissure closure. Ephrin A5 and Eph receptor B2 interaction activates JNK signaling, promoting apoptosis and ensuring proper eye development.

Area of Science:

  • Developmental biology
  • Cell biology
  • Ophthalmology

Background:

  • Eye development relies on a balance between cell division and apoptosis.
  • Apoptosis occurs in the proximoventral optic cup, but its exact role is unclear.

Purpose of the Study:

  • Investigate the role of apoptosis in eye development.
  • Determine the molecular mechanisms regulating optic fissure closure.

Main Methods:

  • Studied the effects of reduced apoptosis in the proximoventral optic cup.
  • Analyzed the expression patterns of ephrin A5 (Efna5) and Eph receptor B2 (Ephb2).
  • Investigated the downstream signaling pathways, including JNK activation.

Main Results:

  • Reduced apoptosis prevented optic fissure closure.
  • Ephrin A5 and Eph receptor B2 expression partially overlapped in the proximoventral optic cup.
  • EphB2 binding to ephrin A5 sustained JNK activation, promoting apoptosis and inhibiting proliferation.

Conclusions:

  • The interaction between EphB2 and ephrin A5 is crucial for regulating apoptosis via JNK signaling.
  • This signaling pathway ensures sufficient progenitor cells for proper optic fissure closure.
  • Cross-subclass Eph/ephrin interactions have evolved to control developmental processes.
Keywords:
ApoptosisMAPKOptic cupOptic fissure closure

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