Appearance of Antigens during Development of the Lens

Those cells of the head ectoderm of chick embryos which are to give rise to the lens show the first signs of differentiation at the 13–16-somite Stage: the nuclei become cylindrical and move gradually toward the base of the cells, while the vacuoles present in the cytoplasm decrease in size and number. During the 16–20-somite stage the changes become clear-cut as the cells transform from a cuboidal to a high cylindrical shape and the nuclei elongate and move perpendicularly to the retinal surface (placode formation; Plate 1, fig. 1b; McKeehan, 1951; Van Doorenmaalen, 1958; Langman et al., 1957). During the 20–30-somite stage the lens placode invaginates and gradually forms a lens vesicle which remains attached to the ectoderm until the 30–31-somite stage, but separates from it at the 32–33-somite stage (lens vesicle formation; Plate 1, figs. 1c, 2b, 2c). At the cellular level it was noted that acidophilic fibres appear in the apical cytoplasm at the 23–24-somite stage.

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The First Appearance of Specific Antigens during the Induction of the Lens1

Development ◽

10.1242/dev.7.2.193 ◽

1959 ◽

Vol 7 (2) ◽

pp. 193-202

Author(s):

Jan Langman

Keyword(s):

Chick Embryo ◽

Direct Contact ◽

Random Distribution ◽

Subsequent Development ◽

Head Region ◽

Retinal Surface ◽

Somite Stage ◽

Specific Antigens ◽

Lens Placode ◽

Placode Formation

The formation of the lens in the chick embryo is known to depend upon ‘inductive’ influences from the eye-cup (Alexander, 1937; Van Deth, 1940; Waddington & Cohen, 1936). A period of direct contact between eye-cup and presumptive lens ectoderm from the 9- to the 20-somite stage is essential for the induction (Weiss, 1947; McKeehan, 1951; Langman, 1956). At the beginning of this period (9–12-somite stage), the cytoplasm of the presumptive lens ectoderm cells is vacuolated and the nuclei have a random distribution, as in the ectodermal epithelium of the head region. During subsequent development (13–16-somite stage) the intracellular vacuoles disappear from the presumptive lens ectoderm and the nuclei become gradually displaced toward the base of the cells in contact with the retinal surface (McKeehan, 1951). At the 16–19-somite stage the cells become more and more columnar (so-called palisading phenomenon) and the nuclei elongated perpendicularly to the basement membrane (lens placode formation).

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A STUDY OF THE INHIBITORY EFFECTS OF CHICK WHOLE EYE EXTRACT ON THE DEVELOPMENT OF THE LENS OF THE CHICK EMBRYO IN VITRO

Canadian Journal of Zoology ◽

10.1139/z66-065 ◽

1966 ◽

Vol 44 (4) ◽

pp. 661-676 ◽

Cited By ~ 1

Author(s):

Robert P. Thompson

Keyword(s):

Chick Embryo ◽

Nutrient Medium ◽

Inhibitory Effect ◽

Reactive System ◽

Vesicle Formation ◽

Inhibitory Effects ◽

Muscle Extract ◽

Lens Vesicle ◽

And Control

To demonstrate the phenomenon of homologous inhibition by clearly interpretable results in a readily reactive system, experiments were carried out to study the effect of chick whole eye extract on the development of the vesicular lens of the chick embryo in vitro. The heads of embryos of 11 through 13 somites were explanted onto nutrient medium diluted with varying amounts of the extract, and cultured for 30 hours. A total of 35 embryos exposed to concentrations of 1:1, 1:2, and 1:4 (extract to medium) showed complete inhibition of lens vesicle formation. Of a total of 53 embryos on concentrations of 1:8, 1:16, 1:32, and 1:64, more than 50% showed inhibition of vesicle formation. The inhibitory effect disappeared at a concentration of 1:128. Control material exposed to some equivalent concentrations of nutrient medium – saline mixtures showed inhibition of vesicle formation in only 15% of 33 embryos. Of a total of 27 control embryos exposed to ventricular muscle extract, approximately one-third showed inhibition of vesicle formation at concentrations of 1:8 and 1:16, with the inhibitory effect disappearing at 1:32. The implications of this result are discussed. Other factors and control experiments are described and their value is assessed.

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The upstream ectoderm enhancer in Pax6 has an important role in lens induction

Development ◽

10.1242/dev.128.22.4415 ◽

2001 ◽

Vol 128 (22) ◽

pp. 4415-4424 ◽

Cited By ~ 3

Author(s):

Patricia V. Dimanlig ◽

Sonya C. Faber ◽

Woytek Auerbach ◽

Helen P. Makarenkova ◽

Richard A. Lang

Keyword(s):

Transcriptional Control ◽

Control Element ◽

Pax6 Gene ◽

Pax6 Expression ◽

Surface Ectoderm ◽

Targeted Deletion ◽

Lens Vesicle ◽

Normal Lens ◽

Lens Formation ◽

Lens Placode

The Pax6 gene has a central role in development of the eye. We show, through targeted deletion in the mouse, that an ectoderm enhancer in the Pax6 gene is required for normal lens formation. Ectoderm enhancer-deficient embryos exhibit distinctive defects at every stage of lens development. These include a thinner lens placode, reduced placodal cell proliferation, and a small lens pit and lens vesicle. In addition, the lens vesicle fails to separate from the surface ectoderm and the maturing lens is smaller and shows a delay in fiber cell differentiation. Interestingly, deletion of the ectoderm enhancer does not eliminate Pax6 production in the lens placode but results in a diminished level that, in central sections, is apparent primarily on the nasal side. This argues that Pax6 expression in the lens placode is controlled by the ectoderm enhancer and at least one other transcriptional control element. It also suggests that Pax6 enhancers active in the lens placode drive expression in distinct subdomains, an assertion that is supported by the expression pattern of a lacZ reporter transgene driven by the ectoderm enhancer. Interestingly, deletion of the ectoderm enhancer causes loss of expression of Foxe3, a transcription factor gene mutated in the dysgenetic lens mouse. When combined, these data and previously published work allow us to assemble a more complete genetic pathway describing lens induction. This pathway features (1) a pre-placodal phase of Pax6 expression that is required for the activity of multiple, downstream Pax6 enhancers; (2) a later, placodal phase of Pax6 expression regulated by multiple enhancers; and (3) the Foxe3 gene in a downstream position. This pathway forms a basis for future analysis of lens induction mechanism.

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Rubella cataract in vitro: Sensitive period of the developing human lens.

Journal of Experimental Medicine ◽

10.1084/jem.141.6.1238 ◽

1975 ◽

Vol 141 (6) ◽

pp. 1238-1248 ◽

Cited By ~ 20

Author(s):

M Karkinen-Jääskeläinen ◽

L Saxén ◽

A Vaheri ◽

P Leinikki

Keyword(s):

Clinical Findings ◽

Lens Capsule ◽

Human Lens ◽

Sensitive Period ◽

Fiber Damage ◽

Viral Antigens ◽

Lens Vesicle ◽

Lens Placode ◽

Made In

The clinically known sensitive period of rubella cataract was studied in vitro by infecting 79 human eye rudiments from embryos aged 4-10 wk with rubella virus. The course of the infection was followed by histological and indirect immunofluorescence methods. Of the rudiments, 12 pairs were in the lens placode or open-lens-vesicle stage, 40 already had closed lens vesicles and in another 27 closed-stage pairs an incision was made in the lens capsule before infection to allow the virus to enter the lens. Uninfected controls differentiated well in vitro for 4-6 wk. The eye rudiments infected in the open-lens-vesicle stage showed lens fiber destruction and viral antigens within the lens. No damage or viral antigens were detected in rudiments infected in the closed stage unless the lens capsule was incisedmwhen this was done, however, fiber damage ensued and viral antigens appeared. The lens capsule was concluded to form a protective barrier around the sensirive fibers at the time of closure of the lens vesicle, confirming the earlier hypothesis and clinical findings.

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Neural tube-ectoderm interactions are required for trigeminal placode formation

Development ◽

10.1242/dev.124.21.4287 ◽

1997 ◽

Vol 124 (21) ◽

pp. 4287-4295 ◽

Cited By ~ 7

Author(s):

M.R. Stark ◽

J. Sechrist ◽

M. Bronner-Fraser ◽

C. Marcelle

Keyword(s):

Neural Crest ◽

Trigeminal Ganglion ◽

Neural Tube ◽

Neural Crest Cells ◽

Surface Ectoderm ◽

Somite Stage ◽

Tissue Interactions ◽

Cranial Neural Crest Cells ◽

Cranial Sensory Ganglia ◽

Placode Formation

Cranial sensory ganglia in vertebrates develop from the ectodermal placodes, the neural crest, or both. Although much is known about the neural crest contribution to cranial ganglia, relatively little is known about how placode cells form, invaginate and migrate to their targets. Here, we identify Pax-3 as a molecular marker for placode cells that contribute to the ophthalmic branch of the trigeminal ganglion and use it, in conjunction with DiI labeling of the surface ectoderm, to analyze some of the mechanisms underlying placode development. Pax-3 expression in the ophthalmic placode is observed as early as the 4-somite stage in a narrow band of ectoderm contiguous to the midbrain neural folds. Its expression broadens to a patch of ectoderm adjacent to the midbrain and the rostral hindbrain at the 8- to 10-somite stage. Invagination of the first Pax-3-positive cells begins at the 13-somite stage. Placodal invagination continues through the 35-somite stage, by which time condensation of the trigeminal ganglion has begun. To challenge the normal tissue interactions leading to placode formation, we ablated the cranial neural crest cells or implanted barriers between the neural tube and the ectoderm. Our results demonstrate that, although the presence of neural crest cells is not mandatory for Pax-3 expression in the forming placode, a diffusible signal from the neuroectoderm is required for induction and/or maintenance of the ophthalmic placode.

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Mechanics of Optic Cup Invagination in the Embryonic Chick Eye

ASME 2012 Summer Bioengineering Conference, Parts A and B ◽

10.1115/sbc2012-80377 ◽

2012 ◽

Author(s):

Alina Oltean ◽

David C. Beebe ◽

Larry A. Taber

Keyword(s):

Eye Development ◽

Embryonic Chick ◽

Optic Vesicle ◽

Surface Ectoderm ◽

Morphogenetic Process ◽

Optic Cup ◽

Optic Vesicles ◽

Lens Vesicle ◽

Lens Placode

Invagination of epithelia is an essential morphogenetic process that occurs in early eye development. The mechanics of the tissue forces necessary for eye invagination are not yet understood [1]. The eyes begin as two optic vesicles that grow outwards from the forebrain and adhere to the surface ectoderm. At this point of contact, both the surface ectoderm and optic vesicle thicken, forming the lens placode and retinal placode, respectively. The two placodes then bend inward to create the lens vesicle and bilayered optic cup (OC) [1, 2].

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Dosage requirement and allelic expression of PAX6 during lens placode formation

Development ◽

10.1242/dev.127.24.5439 ◽

2000 ◽

Vol 127 (24) ◽

pp. 5439-5448 ◽

Cited By ~ 2

Author(s):

C.D. van Raamsdonk ◽

S.M. Tilghman

Keyword(s):

Cell Number ◽

Critical Threshold ◽

Monoallelic Expression ◽

Loss Of Function ◽

Wild Type ◽

Surface Ectoderm ◽

Dosage Requirement ◽

Pax6 Protein ◽

Lens Placode ◽

Placode Formation

Pax6 is a member of the mammalian Pax transcription factor family. Many of the Pax genes display semi-dominant loss-of-function heterozygous phenotypes, yet the underlying cause for this dosage requirement is not known. Mice heterozygous for Pax6 mutations exhibit small eyes (Sey) and in embryos the most obvious defect is a small lens. We have studied lens development in Pax6(Sey)(−1Neu)/+ embryos to understand the basis of the haploinsufficiency. The formation of the lens pre-placode appears to be unaffected in heterozygotes, as deduced from the number of cells, the mitotic index, the amount of apoptosis and the expression of SOX2 and Pax6 in the pre-placode. However, the formation of the lens placode is delayed. The cells at the edge of the lens cup fail to express N-cadherin and undergo apoptosis and the lens fails to detach completely from the surface ectoderm. After formation, the lens, which has 50% of the cells found in wild-type embryos, grows at a rate that is indistinguishable from wild type. We rule out the possibility that monoallelic expression of Pax6 at the time of lens placode formation accounts for the 50% reduction in cell number by showing that expression of Pax6 is biallelic in the lens placode and optic vesicle. We propose instead that a critical threshold of PAX6 protein is required for lens placode formation and that the time in development at which this level is reached is delayed in heterozygotes.

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AP-2α is required after lens vesicle formation to maintain lens integrity

Developmental Dynamics ◽

10.1002/dvdy.24141 ◽

2014 ◽

Vol 243 (10) ◽

pp. 1298-1309 ◽

Cited By ~ 5

Author(s):

Christine L. Kerr ◽

Mizna A. Zaveri ◽

Michael L. Robinson ◽

Trevor Williams ◽

Judith A. West-Mays

Keyword(s):

Vesicle Formation ◽

Lens Vesicle

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Embryology of the teleost (Oncorhynchus mykiss) lens

Canadian Journal of Zoology ◽

10.1139/z94-093 ◽

1994 ◽

Vol 72 (4) ◽

pp. 689-701 ◽

Cited By ~ 2

Author(s):

J. A. West ◽

J. G. Sivak ◽

R. D. Moccia

Keyword(s):

Rainbow Trout ◽

Embryonic Development ◽

Light Microscopy ◽

Oncorhynchus Mykiss ◽

Anterior Pole ◽

Lens Development ◽

Rainbow Trout Oncorhynchus Mykiss ◽

Lens Vesicle ◽

Lens Placode

Embryological studies of the teleost lens have attracted little attention. The morphology of the rainbow trout (Oncorhynchus mykiss) lens during embryonic development was investigated using light microscopy. Results indicate that in general, the embryology of the rainbow trout lens proceeds much like that which has been described for other vertebrates. However, evidence in this study indicates that both layers of the lens placode invaginate, forming a lens pit, contradicting earlier descriptions of lens development in fishes. Furthermore, a hollow lens vesicle does not appear during development, as is typically described for the mammalian lens. Most importantly, the posterior limit of the anterior epithelium is situated well beyond the equator, three-quarters of the distance from the anterior pole of the lens. As a result, the germinative and transitional zones are located more posteriorly than traditionally described. The consequence of these features and their relevance to the shape of the lens are discussed.

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