Mitotic Position and Morphology of Committed Precursor Cells in the Zebrafish Retina Adapt to Architectural Changes upon Tissue Maturation

Weber, Isabell P.; Ramos, Ana Patricia; Strzyz, Paulina; Leung, Louis C.; Young, Stephen; Norden, Caren

doi:10.1016/j.celrep.2014.03.014

Cited by 69 publications

(112 citation statements)

References 29 publications

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“…To test this notion, we performed HS on transgenic embryos at 48 hpf. At this stage, neurogenesis peaks, and only few proliferative divisions remain (Weber et al, 2014). Indeed, in these fish, retinal development was not significantly impaired: all retinal layers were formed, largely resembling control retinae, and only minor defects could be observed ( Figures 6I [N amplification is cell proliferation.…”

Section: Centriole Amplification Affects the Proliferative Phase Of Rmentioning

confidence: 91%

“…Crossing OS-Plk4 fish to transgenic lines labeling both early (Ath5-gapRFP marker for retinal ganglion and photoreceptors) and later-born neurons (Ptf1A-GFP marker for amacrine and horizontal cells and Vsx1-GFP marker for bipolar cells) (Weber et al, 2014) revealed that OS-Plk4-expressing cells were able to differentiate into all neuronal subtypes (Figures 6E and 6F). To test whether this was also the case upon mosaic expression, we injected the HS-OS-Plk4 construct together with the HS-H2B-GFP to label Plk4-expressing cells.…”

Section: Centriole Amplification Affects the Proliferative Phase Of Rmentioning

confidence: 94%

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Centriole Amplification in Zebrafish Affects Proliferation and Survival but Not Differentiation of Neural Progenitor Cells

et al. 2015

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In animal cells, supernumerary centrosomes, resulting from centriole amplification, cause mitotic aberrations and have been associated with diseases, including microcephaly and cancer. To evaluate how centriole amplification impacts organismal development at the cellular and tissue levels, we used the in vivo imaging potential of the zebrafish. We demonstrate that centriole amplification can induce multipolar anaphase, resulting in binucleated cells. Such binucleation causes substantial apoptosis in the neuroepithelium. Interestingly, not all epithelia are similarly sensitive to binucleation, as skin cells tolerate it without entering apoptosis. In the neuroepithelium, however, binucleation leads to tissue degeneration and subsequent organismal death. Notably, this tissue degeneration can be efficiently counterbalanced by compensatory proliferation of wild-type cells. Because the risk for generating a binucleated daughter recurs at every cell division, centriole amplification in the neuroepithelium is especially deleterious during progenitor proliferation. Once cells reach the differentiation phase, however, centriole amplification does not impair neuronal differentiation.

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Section: Centriole Amplification Affects the Proliferative Phase Of Rmentioning

confidence: 91%

Section: Centriole Amplification Affects the Proliferative Phase Of Rmentioning

confidence: 94%

Centriole Amplification in Zebrafish Affects Proliferation and Survival but Not Differentiation of Neural Progenitor Cells

et al. 2015

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“…Spatial restrictions due to the maintained presence of intact photoreceptors following inner retinal cell death by ouabain exposure could explain the relatively lower migration potential of Müller glia nuclei into the ONL compared to the light-damaged retina lacking photoreceptors. Similarly, NPC divisions in the developing retina change from apical to non-apical at the onset of ONL formation (Weber et al 2014), supporting that cell density restrictions at least partially determine the position of mitosis.…”

Section: Müller Glia Inmmentioning

confidence: 96%

Interkinetic Nuclear Migration in the Regenerating Retina

Lahne

Hyde

2015

Retinal Degenerative Diseases

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In the adult zebrafish, death of retinal neurons stimulates Müller glia to re-enter the cell cycle to produce neuronal progenitor cells (NPCs) that undergo further cell divisions and differentiate to replace lost neurons in the correct spatial locations. Understanding the mechanisms regulating retinal regeneration will ultimately provide avenues to overcome vision loss in human. Recently, the observation of interkinetic nuclear migration (INM) of Müller glia in the regenerating zebrafish retina resulted in the inclusion of an additional complex step to the regeneration process. The pathways regulating INM and its function in the regenerating retina have not been well studied. Here, we summarize the evidence for INM in the regenerating retina and review mechanisms that control INM during neuro-epithelial development in the context of pathways known to be critical during retinal regeneration.

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“…18 , which has previously been used to inhibit in vivo cell proliferation in the embryonic retina 19 . In BI2536-treated brains, the nuclear density rostral to the OT and thus the cell density gradient was significantly decreased compared to controls, particularly at later stages (Fig.…”

Section: A B) (See Online Methods For Details)mentioning

confidence: 99%

“…2e). To test if local cell densities drive the evolution of the stiffness gradient during OT turning, we repeated both nuclear staining and tiv-AFM measurements on embryos treated with the mitotic blocker BI253618 , which has previously been used to inhibit in vivo cell proliferation in the embryonic retina 19 . In BI2536-treated brains, the nuclear density rostral to the OT and thus the cell density gradient was significantly decreased compared to controls, particularly at later stages (Fig.…”

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confidence: 99%

Simultaneous in vivo time-lapse stiffness mapping and fluorescence imaging of developing tissue

Thompson

Pillai

Dimov

et al. 2018

Preprint

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Tissue mechanics is important for development; however, the spatio-temporal dynamics of in vivo tissue stiffness is still poorly understood. We here developed tiv-AFM, combining time-lapse in vivo atomic force microscopy with upright fluorescence imaging of embryonic tissue, to show that in the developing Xenopus brain, a stiffness gradient evolves over time because of differential cell proliferation. Subsequently, axons turn to follow this gradient, underpinning the importance of timeresolved mechanics measurements.. CC-BY-NC-ND 4.0 International license It is made available under a (which was not peer-reviewed) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. 1).A fluorescence zoom stereomicroscope equipped with an sCMOS camera (quantum yield 82%)were custom-fitted above a bio-AFM set-up ( Supplementary Fig. 1), which had a transparent pathway along the area of the cantilever. To cope with the long working distances required for imaging through the AFM head, the microscope was fitted with a 0.125 NA / 114 mm WD objective.The AFM was set up on an automated motorised stage containing a temperature-controlled sample holder to maintain live specimens at optimal conditions during the experimental time course. (Fig. 1a, b) (see online methods for details).We tested tiv-AFM using the developing Xenopus embryo brain during outgrowth of the optic tract (OT) as a model (Fig. 1c). In the OT, retinal ganglion cell axons grow in a bundle across the brain surface, making a stereotypical turn in the caudal direction en route that directs them to their target, the visual centre of the brain 13 . We previously demonstrated that by later stages of OT outgrowth (i.e. when axons had reached their target), a local stiffness gradient lies orthogonal to the path of OT axons, with the stiffer region rostral to the OT and softer region caudal to it 2 . This gradient strongly correlated with axon turning, with the OT routinely turning caudally towards softer tissue 2 .We therefore wanted to determine when this stiffness gradient first developed, whether its emergence preceded OT axon turning, and what the origin of that stiffness gradient was.To answer these questions, we performed iterated tiv-AFM measurements of the embryonic brain in vivo at early-intermediate stages, i.e. just before and during turn initiation by the first 'pioneer' OT axons. The apparent elastic modulus K, which is a measure of the tissue's elastic stiffness, was assessed in a ~150 µm by 250 µm raster at 20 µm resolution every ~35 minutes, producing a sequence of 'stiffness maps' of the area (Supplementary Fig. 2). To reduce noise, raw . CC-BY-NC-ND 4.0 International license It is made available under a (which was not peer-reviewed) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity.The 17, 2018; AFM data were interpolated and smoothed in x-, y-, and time dimensions using an algorithm based on the discrete cosine transform (Fig. 1d, see online methods for details)...

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Mitotic Position and Morphology of Committed Precursor Cells in the Zebrafish Retina Adapt to Architectural Changes upon Tissue Maturation

Cited by 69 publications

References 29 publications

Centriole Amplification in Zebrafish Affects Proliferation and Survival but Not Differentiation of Neural Progenitor Cells

Centriole Amplification in Zebrafish Affects Proliferation and Survival but Not Differentiation of Neural Progenitor Cells

Interkinetic Nuclear Migration in the Regenerating Retina

Simultaneous in vivo time-lapse stiffness mapping and fluorescence imaging of developing tissue

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