June 2015
Volume 56, Issue 7
ARVO Annual Meeting Abstract  |   June 2015
Cell−ECM interactions during formation of the zebrafish hyaloid vasculature
Author Affiliations & Notes
  • Andrea Hartsock
    Biological Sciences, University of Texas, Austin, Austin, TX
  • Victoria Arnold
    Biological Sciences, University of Texas, Austin, Austin, TX
  • Jeffrey Gross
    Biological Sciences, University of Texas, Austin, Austin, TX
  • Footnotes
    Commercial Relationships Andrea Hartsock, None; Victoria Arnold, None; Jeffrey Gross, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 899. doi:
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      Andrea Hartsock, Victoria Arnold, Jeffrey Gross; Cell−ECM interactions during formation of the zebrafish hyaloid vasculature. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):899.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: Vasculature formation requires an orchestrated series of morphogenetic changes to generate an integrated vessel system. Previous work by our laboratory demonstrated there are three stages of hyaloid development in zebrafish: Stage I- arrival of hyaloid cells at the lens and formation of the hyaloid loop, Stage II- formation of a branched hyaloid network, and Stage III- refinement of the hyaloid network (Hartsock et al., 2014). The lens is not required for recruitment of hyaloid precursor cells, but is required for Stage II and III development and maturation. The lens is surrounded by the lens capsule, an ECM-rich basement membrane. It is not known how the ECM of the lens capsule contributes to hyaloid formation. Here, we test the hypothesis that distinct cell-ECM interactions play an integral role in building the hyaloid.

Methods: Fixed sample and in vivo time lapse imaging of fli1a:GFP (a hyaloid marker) were performed in a variety of zebrafish lines possessing mutations in ECM components or their cellular interaction partners: lamining1 (lamc1), fibronectin1b (fn1b), integrin a5 (itga5), and integrin b1 (itgb1). All images were processed as maximum projections via ImageJ.

Results: in vivo time-lapse imaging revealed that mutations in all cell-ECM components resulted in Stage II and III hyaloid defects. Unique defects were identified in each mutant. For example, Stage II hyaloid network branching was disrupted in lamc1 and fn1b mutants; fn1b mutants possessed clumps of vascular precursor cells on the lens that did not organize into mature vessels. itga5 mutants also possessed Stage II defects, with vessels that were reduced in branch number and thickness. Stage III, refinement of the vascular network appeared normal in itga5 and itgb1 mutants, but not in fn1b or lamc1 mutants.

Conclusions: Analysis of hyaloid formation in cell-ECM component mutants revealed requirements for these proteins during hyaloid development. Mutations in ECM components (fn1b, lamc1) were more severe, likely affecting multiple cellular interacting partners. Conversely, hyaloid defects in mutants affecting the interacting partners (itga5, itgb1) were more limited, suggesting specific roles for these in distinct phases of hyaloid development. Further analyses of downstream regulators of these cell-ECM pathways will generate a comprehensive understanding of the cellular underpinnings of hyaloid morphogenesis during embryonic eye development.


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