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Icha, J.

Publications and source records attributed to Icha, J..

2 recordsLinked to original sources

Bidirectional neuronal migration coordinates retinal morphogenesis bypreventing spatial competition

While the design of industrial products is often optimized for the sequential assembly of single components, organismal development is hallmarked by the concomitant occurrence of tissue growth and organization. Often this means that proliferating and differentiating cells occur at the same time in a shared tissue environment that continuously changes. How cells adapt to architectural changes in order to prevent spatial interference remains unclear. To understand how cell movements important for growth and organization are orchestrated, we here study the emergence of photoreceptor neurons that occur during the peak of retinal growth using zebrafish, human tissue and human organoids. Quantitative imaging reveals that successful retinal morphogenesis depends on active bidirectional photoreceptor translocation. This leads to a transient transfer of the entire cell population away from the apical proliferative zone. This migration pattern is driven by distinct cytoskeletal machineries, depending on direction: microtubules are required for basal translocation, while actomyosin drives apical movement. Blocking photoreceptor translocation leads to apical overcrowding that hampers progenitor movements. Thus, photoreceptor migration is crucial to prevent competition for space and thereby allows concurrent tissue growth and lamination. This shows that neuronal migration, in addition to its canonical role in cell positioning, is involved in coordinating morphogenesis.

developmental biology↗

Conditional control of fluorescent protein degradation by an auxin-dependent nanobody

The conditional and reversible depletion of proteins by auxin-mediated degradation is a powerful tool to investigate protein functions in cells and whole organisms. However, its wider applications require fusing the auxin-inducible degron (AID) to individual target proteins. Thus, establishing the auxin system for multiple proteins can be challenging. Another approach for directed protein degradation are anti-GFP nanobodies, which can be applied to GFP stock collections that are readily available in different experimental models. Here, we combine the advantages of auxin and nanobody-based degradation technologies creating an AID-nanobody to degrade GFP-tagged proteins at different cellular structures in a conditional and reversible manner in human cells. We demonstrate efficient and reversible inactivation of the anaphase promoting complex/cyclosome (APC/C) and thus provide new means to study the functions of this essential ubiquitin E3 ligase. Further, we establish auxin degradation in a vertebrate model organism by employing AID-nanobodies in zebrafish.

cell biology↗