Par3 in chick lens placode development

genesis ◽  
2017 ◽  
Vol 55 (6) ◽  
pp. e23032 ◽  
Author(s):  
Maraysa de Oliveira Melo ◽  
Ricardo Moraes Borges ◽  
Chao Yun Irene Yan
Keyword(s):  

2011 ◽  
Vol 356 (1) ◽  
pp. 149-150
Author(s):  
Maraysa Melo ◽  
Ricardo Moraes Borges ◽  
Chao Yun Irene Yan
Keyword(s):  


2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Zhen Li ◽  
Sumin Gu ◽  
Yumeng Quan ◽  
Kulandaiappan Varadaraj ◽  
Jean X. Jiang

AbstractCongenital cataracts are associated with gene mutations, yet the underlying mechanism remains largely unknown. Here we reported an embryonic chick lens model that closely recapitulates the process of cataract formation. We adopted dominant-negative site mutations that cause congenital cataracts, connexin, Cx50E48K, aquaporin 0, AQP0R33C, αA-crystallin, CRYAA R12C and R54C. The recombinant retroviruses containing these mutants were microinjected into the occlusive lumen of chick lenses at early embryonic development. Cx50E48K expression developed cataracts associated with disorganized nuclei and enlarged extracellular spaces. Expression of AQP0R33C resulted in cortical cataracts, enlarged extracellular spaces and distorted fiber cell organization. αA crystallin mutations distorted lens light transmission and increased crystalline protein aggregation. Together, retroviral expression of congenital mutant genes in embryonic chick lenses closely mimics characteristics of human congenital cataracts. This model will provide an effective, reliable in vivo system to investigate the development and underlying mechanism of cataracts and other genetic diseases.



1970 ◽  
Vol 117 (3) ◽  
pp. 63P-63P ◽  
Author(s):  
Ruth M. Clayton ◽  
D. E. S. Truman ◽  
J. C. Campbell


2007 ◽  
Vol 75 (8) ◽  
pp. 737-744 ◽  
Author(s):  
Hasan Mahmud Reza ◽  
Hirofumi Nishi ◽  
Kohsuke Kataoka ◽  
Yoshiko Takahashi ◽  
Kunio Yasuda


1978 ◽  
Vol 65 (2) ◽  
pp. 372-382 ◽  
Author(s):  
Iain Thomson ◽  
Christine E. Wilkinson ◽  
James F. Jackson ◽  
David I. de Pomerai ◽  
Ruth M. Clayton ◽  
...  


1968 ◽  
Vol 17 (5) ◽  
pp. 544-561 ◽  
Author(s):  
Sohan P. Modak ◽  
Georgia Morris ◽  
Tuneo Yamada


1980 ◽  
Vol 339 (1 Growth Regula) ◽  
pp. 265-279 ◽  
Author(s):  
Joram Piatigorsky ◽  
Toshimichi Shinohara ◽  
Suraj P. Bhat ◽  
Rosalie Reszelbach ◽  
Raymond E. Jones ◽  
...  


Development ◽  
2000 ◽  
Vol 127 (5) ◽  
pp. 945-956 ◽  
Author(s):  
J.M. Collinson ◽  
R.E. Hill ◽  
J.D. West

Chimaeric mice were made by aggregating Pax6(−/−) and wild-type mouse embryos, in order to study the interaction between the optic vesicle and the prospective lens epithelium during early stages of eye development. Histological analysis of the distribution of homozygous mutant cells in the chimaeras showed that the cell-autonomous removal of Pax6(−/−) cells from the lens, shown previously at E12.5, is nearly complete by E9.5. Most mutant cells are eliminated from an area of facial epithelium wider than, but including, the developing lens placode. This result suggests a role for Pax6 in maintaining a region of the facial epithelium that has the tissue competence to undergo lens differentiation. Segregation of wild-type and Pax6(−/−) cells occurs in the optic vesicle at E9.5 and is most likely a result of different adhesive properties of wild-type and mutant cells. Also, proximo-distal specification of the optic vesicle (as assayed by the elimination of Pax6(−/−) cells distally), is disrupted in the presence of a high proportion of mutant cells. This suggests that Pax6 operates during the establishment of patterning along the proximo-distal axis of the vesicle. Examination of chimaeras with a high proportion of mutant cells showed that Pax6 is required in the optic vesicle for maintenance of contact with the overlying lens epithelium. This may explain why Pax6(−/−) optic vesicles are inefficient at inducing a lens placode. Contact is preferentially maintained when the lens epithelium is also wild-type. Together, these results demonstrate requirements for functional Pax6 in both the optic vesicle and surface epithelia in order to mediate the interactions between the two tissues during the earliest stages of eye development.



Development ◽  
1963 ◽  
Vol 11 (4) ◽  
pp. 683-688
Author(s):  
F. Peetoom ◽  
W. J. A. TH. Kraijenhoff Sloot ◽  
M. W. Woerdeman

The use of specific antisera against different embryonic antigens to detect a correlation between morphological and immunochemical differentiation in ontogenesis has proved to be a valuable technique. In a study of the appearance of lens proteins in chick embryos, using various antisera and agar precipitation methods, we observed the development of precipitation lines which did not correspond to specific lens proteins. These lines were encountered in the Ouchterlony and immunoelectrophoretic pictures obtained with young (up to 120 hr.) embryo or lens extracts when these were tested with antiserum to 24-hr, embryo extract or to adult chick serum. However, this type of precipitation band was never found when antiserum against adult chick lens was used. Some of our experimental results which clarify the nature of these precipitation reactions are summarized below. Full details of these experiments are the subject of another publication.



Development ◽  
2001 ◽  
Vol 128 (22) ◽  
pp. 4415-4424 ◽  
Author(s):  
Patricia V. Dimanlig ◽  
Sonya C. Faber ◽  
Woytek Auerbach ◽  
Helen P. Makarenkova ◽  
Richard A. Lang

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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