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Zonular defects in loxl1-deficient zebrafish.

Min Zhang1,2,3, Shaoyang Sun4, Lei Wang4

  • 1Department of Ophthalmology and Vision Science, Eye & ENT Hospital, Fudan University, Shanghai, China.

Clinical & Experimental Ophthalmology
|September 29, 2021
PubMed
Summary

Lysyl oxidase-like 1 (loxl1) deficiency in zebrafish causes zonular defects and particle accumulation, mimicking exfoliation syndrome (XFS) ocular pathology. This loxl1-deficient zebrafish model offers a promising avenue for studying XFS.

Keywords:
LOXL1exfoliation syndromelens subluxationzebrafishzonules

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Area of Science:

  • Ophthalmology
  • Genetics
  • Developmental Biology

Background:

  • Exfoliation syndrome (XFS) is a common cause of secondary glaucoma.
  • The role of lysyl oxidase-like 1 (loxl1) in ocular development and XFS pathogenesis is not fully understood.

Purpose of the Study:

  • To investigate the function of the loxl1 gene in zebrafish eye development.
  • To determine if loxl1 deficiency can model the ocular features of XFS.

Main Methods:

  • CRISPR/Cas9 technology was used to create loxl1 gene mutations in zebrafish.
  • Ocular structures and gene expression were analyzed in wildtype and mutant zebrafish at various developmental stages.

Main Results:

  • Zebrafish with loxl1 deficiency exhibited abnormal zonular bundling and accumulation of pearl-like particles.
  • Mutant zebrafish showed thinning or loss of elastic lamina in Bruch's membrane and breakage in homozygous mutants.
  • loxl1 deficiency led to significant structural changes in the zebrafish eye, including zonular defects and Bruch's membrane abnormalities.

Conclusions:

  • The loxl1-deficient zebrafish exhibits ocular pathologies relevant to XFS.
  • This zebrafish model is valuable for further research into XFS zonular pathology.