Aldehyde dehydrogenase is a positional marker in the retina

Development ◽  
1991 ◽  
Vol 112 (3) ◽  
pp. 693-702 ◽  
Author(s):  
P. McCaffery ◽  
P. Tempst ◽  
G. Lara ◽  
U.C. Drager
Keyword(s):  
Aldehyde Dehydrogenase ◽  
Adult Mouse ◽  
Mouse Retina ◽  
Retinal Position ◽  
Embryonic Mouse ◽  
Undifferentiated Cells ◽  
Positional Marker ◽  
Optic Axons ◽  
Asymmetrically Distributed ◽  
Dorsal Retina

An asymmetrically distributed protein in the embryonic mouse retina was identified as an aldehyde dehydrogenase through protein microsequencing. It was characterized as a cytosolic isoform with basic isoelectric point and preference for aliphatic substrates, features that resemble those of the isoform AHD-2 which is known to oxidize retinaldehyde to retinoic acid. Immunohistochemistry with aldehyde dehydrogenase antisera showed strong labeling of the dorsal retina from the early eye vesicle stage into adulthood. In addition, optic axons originating from the dorsal retina were transiently labeled during their outgrowth phase. Whereas in the embryo the enzyme was expressed in undifferentiated cells and in neurons, in the retina of the adult mouse the asymmetrically distributed isoform was mainly expressed in Muller glia, with the number of labeled glial cells varying with retinal position.

The guidance of optic axons in the developing and adult mouse retina

1979 ◽  
Vol 193 (4) ◽  
pp. 763-773 ◽  
Author(s):  
Stephen Goldberg ◽  
Beryn Frank
Keyword(s):  
Adult Mouse ◽  
Mouse Retina ◽  
Optic Axons

The early development of retinal ganglion cells with uncrossed axons in the mouse: retinal position and axonal course

Development ◽  
1990 ◽  
Vol 108 (3) ◽  
pp. 515-523 ◽  
Author(s):  
R.J. Colello ◽  
R.W. Guillery
Keyword(s):  
Developmental Stages ◽  
Ganglion Cells ◽  
Optic Chiasm ◽  
Temporal Part ◽  
Retinal Ganglion ◽  
Retinal Position ◽  
Optic Stalk ◽  
Carbocyanine Dye ◽  
Optic Axons ◽  
Dorsal Retina

The carbocyanine dye, DiI, has been used to study the retinal origin of the uncrossed retinofugal component of the mouse and to show the course taken by these fibres through the optic nerve and chiasm during development. Optic axons first arrive at the chiasm at embryonic day 13 (E13) but do not cross the midline until E14. After this stage, fibres taking an uncrossed course can be selectively labelled by unilateral tract implants of DiI. The earliest ipsilaterally projecting ganglion cells are located in the dorsal central retina. The first sign of the adult pattern of distribution of ganglion cells with uncrossed axons located mainly in the ventrotemporal retina is seen on embryonic day 16.5, thus showing that the adult line of decussation forms early in development. A small number of labelled cells continue to be found in nasal and dorsal retina at all later stages. At early stages (E14-15), retrogradely labelled uncrossed fibres are found in virtually all fascicles of the developing nerve, intermingling with crossed axons throughout the length of the nerve. At later stages of development (E16-17), although uncrossed fibres pass predominantly within the temporal part of the stalk, they remain intermingled with crossed axons. A significant number of uncrossed axons also lie within the nasal part of the optic stalk. The position of uncrossed fibres throughout the nerve in the later developmental stages is comparable to that seen in the adult rodent (Baker and Jeffery, 1989). The distribution of uncrossed axons thus indicates that positional cues are not sufficient to account for the choice made by axons when they reach the optic chiasm.

Abstract 860: Phenotypic Characterization Of Murine And Human Cardiac-resident Progenitor Cells Isolated On Basis Of Aldehyde-dehydrogenase Activity

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Albert Spicher ◽  
Andrea Meinhardt ◽  
Marc-Estienne Roehrich ◽  
Giuseppe Vassalli
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Progenitor Cells ◽  
Aldehyde Dehydrogenase ◽  
Adult Mouse ◽  
Heart Cells ◽  
Stem Cell Markers ◽  
Aldh Activity ◽  
Differentiation Potential ◽  
Cellular Property

Identification of stem cells based on hematopoietic stem cell (HSC) surface markers, such as stem cell antigen-1 (Sca-1) and the c-kit receptor, has limited specificity. High aldehyde-dehydrogenase (ALDH) activity is a general cellular property of stem cells shared by HSC, neural, and intestinal stem cells. The presence of cells with high ALDH activity in the adult heart has not been investigated. Methods: Cells were isolated from adult mouse hearts, and from atrial appendage samples from humans with ischemic or valvular heart disease. Myocyte-depleted mouse Sca-1+, and lineage (Lin)-negative/c-kit+ human heart cells were purified with immunomagnetic beads. ALDH-high cells were identified using a specific fluorescent substrate, and sorted by FACS. Cell surface marker analysis was performed by flow cytometry. Results: Myocyte-depleted mouse heart cells contained 4.8+/−3.2% ALDH-high/SSC-low and 32.6+/−1.6% Sca-1+ cells. ALDH-high cells were Lin-negative, Sca-1+ CD34+ CD105+ CD106+, contained small CD44+ (27%) and CD45+ (15%) subpopulations, and were essentially negative for c-kit (2%), CD29, CD31, CD133 and Flk-1. After several passages in culture, ~20% of ALDH-high cells remained ALDH-high. Myocyte-depleted human atrial cells contained variable numbers of ALDH-high cells ranging from 0.5% to 11%, and 4% Lin-negative/c-kit+ cells. ALDH-high cells were CD29+ CD105+, contained a small c-kit+ subpopulation (5%), and were negative for CD31, CD45 and CD133. After 5 passages in culture, the majority of ALDH-high cells remained ALDH-high. Conclusions: Adult mouse and human hearts contain significant numbers of cells with high ALDH activity, a general cellular property that stem cells possess in different organs, and express stem cell markers (Sca-1 and CD34 in the mouse). The immunophenotype of cardiac-resident ALDH-high cells differs from that previously described for bone marrow ALDH-high HSC, and suggests that this cell population may be enriched in mesenchymal progenitors. Analysis of lineage differentiation potential of ALDH-high cells is in progress. ALDH activity provides a new, practical approach to purifying cardiac-resident progenitor cells.

Lineage-specific morphogenesis in the developing pancreas: role of mesenchymal factors

Development ◽  
1996 ◽  
Vol 122 (2) ◽  
pp. 439-447 ◽  
Author(s):  
G.K. Gittes ◽  
P.E. Galante ◽  
D. Hanahan ◽  
W.J. Rutter ◽  
H.T. Debase
Keyword(s):  
Basement Membrane ◽  
Adult Mouse ◽  
Renal Capsule ◽  
Pancreatic Development ◽  
Embryonic Mouse ◽  
Cell Lineages ◽  
Ductal Cell ◽  
Pancreatic Epithelium ◽  
Embryonic Epithelium

Pancreatic organogenesis has been a classic example of epitheliomesenchymal interactions. The nature of this interaction, and the way in which endocrine, acinar and ductal cell lineages are generated from the embryonic foregut has not been determined. It has generally been thought that mesenchyme is necessary for all aspects of pancreatic development. In addition islets have been thought to derive, at least in part, from ducts. We microdissected 11-day embryonic mouse pancreas and developed several culture systems for assays of differentiation: (i) on transparent filters; (ii) suspended in a collagen I gel; (iii) suspended in a basement membrane rich gel; (iv) under the renal capsule of an adult mouse. Epithelia were grown either with or without mesenchyme, and then assayed histologically and immunohistochemically. Epithelium with its mesenchyme (growth systems i-iv) always grew into fully differentiated pancreas (acinar, endocrine, adn ductal elements). In the basement membrane-rich gel, epithelium without mesenchyme formed ductal structures. Under the renal capsule of the adult mouse the epithelium without mesenchyme exclusively formed clusters of mature islets. These latter results represent the first demonstration of pure islets grown from early pancreatic precursor cells. In addition, these islets seemed not to have originated from ducts. We propose that the default path for growth of embryonic pancreatic epithelium is to form islets. In the presence of basement membrane constituents, however, the pancreatic analage epithelium appears to be programmed to form ducts. Mesenchyme seems not to be required for all aspects of pancreatic development, but rather only for the formation of acinar structures. In addition, the islets seem to form from early embryonic epithelium (which only express non-acinar genes). This formation occurs without any specific embryonic signals, and without any clear duct or acinus formation.

scholarly journals STAT pathway activation limits the Ascl1-mediated chromatin remodeling required for neural regeneration from Müller glia in adult mouse retina

2019 ◽  
Author(s):  
Nikolas L. Jorstad ◽  
Matthew S. Wilken ◽  
Levi Todd ◽  
Paul Nakamura ◽  
Nick Radulovich ◽  
...  
Keyword(s):  
Adult Mouse ◽  
Neural Regeneration ◽  
Mouse Retina ◽  
Binding Motif ◽  
Muller Glia ◽  
Müller Glia ◽  
Rna Seq ◽  
Transgenic Expression ◽  
Pathway Activation ◽  
Stat Pathway

AbstractMüller glia can serve as a source for retinal regeneration in some non-mammalian vertebrates. Recently we found that this process can be induced in mouse Müller glia after injury, by combining transgenic expression of the proneural transcription factor Ascl1 and the HDAC inhibitor TSA. However, new neurons are only generated from a subset of Müller glia in this model, and identifying factors that limit Ascl1-mediated MG reprogramming could potentially make this process more efficient, and potentially useful clinically. One factor that limits neurogenesis in some non-mammalian vertebrates is the STAT pathway activation that occurs in Müller glia in response to injury. In this report, we tested whether injury induced STAT activation hampers the ability of Ascl1 to reprogram Müller glia into retinal neurons. Using a STAT inhibitor, in combination with our previously described reprogramming paradigm, we found a large increase in the ability of Müller glia to generate neurons, similar to those we described previously. Single-cell RNA-seq showed that the progenitor-like cells derived from Ascl1-expressing Müller glia have a higher level of STAT signaling than those that become neurons. Using Ascl1 ChIP-seq and DNase-seq, we found that developmentally inappropriate Ascl1 binding sites (that were unique to the overexpression context) had enrichment for the STAT binding motif. This study provides evidence that STAT pathway activation reduces the efficiency of Ascl1-mediated reprogramming in Müller glia, potentially by directing Ascl1 to inappropriate targets.

scholarly journals Pan-Retinal Characterisation of Light Responses from Ganglion Cells in the Developing Mouse Retina

2016 ◽  
Author(s):  
Gerrit Hilgen ◽  
Sahar Pirmoradian ◽  
Daniela Pamplona ◽  
Pierre Kornprobst ◽  
Bruno Cessac ◽  
...  
Keyword(s):  
Large Scale ◽  
Ganglion Cells ◽  
Mouse Retina ◽  
Multielectrode Array ◽  
Retinal Ganglion ◽  
Developmental Profile ◽  
Light Responses ◽  
Ecological Requirements ◽  
Eye Opening ◽  
Dorsal Retina

AbstractWe have investigated the ontogeny of light-driven responses in mouse retinal ganglion cells (RGCs). Using a large-scale, high-density multielectrode array, we recorded from hundreds to thousands of RGCs simultaneously at pan-retinal level, including dorsal and ventral locations. Responses to different contrasts not only revealed a complex developmental profile for ON, OFF and ON-OFF RGC types, but also unveiled differences between dorsal and ventral RGCs. At eye-opening, dorsal RGCs of all types were more responsive to light, perhaps indicating an environmental priority to nest viewing for pre-weaning pups. The developmental profile of ON and OFF RGCs exhibited antagonistic behavior, with the strongest ON responses shortly after eye-opening, followed by an increase in the strength of OFF responses later on. Further, we found that with maturation receptive field (RF) center sizes decrease, responses to light get stronger, and centers become more circular while seeing differences in all of them between RGC types. These findings show that retinal functionality is not spatially homogeneous, likely reflecting ecological requirements that favour the early development of dorsal retina, and reflecting different roles in vision in the mature animal.

scholarly journals Kinase independent function of EphB receptors in retinal axon pathfinding to the optic disc from dorsal but not ventral retina

Development ◽  
2000 ◽  
Vol 127 (6) ◽  
pp. 1231-1241 ◽  
Author(s):  
E. Birgbauer ◽  
C.A. Cowan ◽  
D.W. Sretavan ◽  
M. Henkemeyer
Keyword(s):  
Optic Disc ◽  
Tyrosine Kinases ◽  
Receptor Tyrosine Kinases ◽  
Retinal Development ◽  
Mouse Retina ◽  
Target Cells ◽  
Eph Receptors ◽  
Axon Pathfinding ◽  
Embryonic Mouse ◽  
Ephb Receptors

Optic nerve formation requires precise retinal ganglion cell (RGC) axon pathfinding within the retina to the optic disc, the molecular basis of which is not well understood. At CNS targets, interactions between Eph receptor tyrosine kinases on RGC axons and ephrin ligands on target cells have been implicated in formation of topographic maps. However, studies in chick and mouse have shown that both Eph receptors and ephrins are also expressed within the retina itself, raising the possibility that this receptor-ligand family mediates aspects of retinal development. Here, we more fully document the presence of specific EphB receptors and B-ephrins in embryonic mouse retina and provide evidence that EphB receptors are involved in RGC axon pathfinding to the optic disc. We find that as RGC axons begin this pathfinding process, EphB receptors are uniformly expressed along the dorsal-ventral retinal axis. This is in contrast to the previously reported high ventral-low dorsal gradient of EphB receptors later in development when RGC axons map to CNS targets. We show that mice lacking both EphB2 and EphB3 receptor tyrosine kinases, but not each alone, exhibit increased frequency of RGC axon guidance errors to the optic disc. In these animals, major aspects of retinal development and cellular organization appear normal, as do the expression of other RGC guidance cues netrin, DCC, and L1. Unexpectedly, errors occur in dorsal but not ventral retina despite early uniform or later high ventral expression of EphB2 and EphB3. Furthermore, embryos lacking EphB3 and the kinase domain of EphB2 do not show increased errors, consistent with a guidance role for the EphB2 extracellular domain. Thus, while Eph kinase function is involved in RGC axon mapping in the brain, RGC axon pathfinding within the retina is partially mediated by EphB receptors acting in a kinase-independent manner.

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