scholarly journals Interaction of major intrinsic protein (aquaporin-0) with fiber connexins in lens development

2004 ◽  
Vol 117 (6) ◽  
pp. 871-880 ◽  
Author(s):  
X. S. Yu
2005 ◽  
Vol 280 (23) ◽  
pp. 22081-22090 ◽  
Author(s):  
Xun Sean Yu ◽  
Xinye Yin ◽  
Eileen M. Lafer ◽  
Jean X. Jiang

The eye lens is dependent upon a network of gap junction-mediated intercellular communication to facilitate its homeostasis and development. Three gap junction-forming proteins are expressed in the lens of which two are in lens fibers, namely connexin (Cx) 45.6 and 56. Major intrinsic protein (MIP), also known as aquaporin-0 (AQP0), is the most abundant membrane protein in lens fibers. However, its role in the lens is not clear. Our previous studies show that MIP(AQP0) associates with gap junction plaques formed by Cx45.6 and Cx56 during the early stages of embryonic chick lens development but not in late embryonic and adult lenses. We report here that MIP(AQP0) directly interacts with Cx45.6 but not with Cx56. We further identified the intracellular loop of Cx45.6 as the interacting domain for the MIP(AQP0) C terminus. Surface plasmon resonance experiments indicated that the C-terminal domain of MIP(AQP0) interacts with two binding sites within the intracellular loop region of Cx45.6 with a KD(app) of 7.5 and 10.3 μm, respectively. The KD(app) for the full-length loop region is 7.7 μm. The cleavage at the intracellular loop of Cx45.6 was observed during lens development, and the C terminus of MIP(AQP0) did not interact with the loop-cleaved form of Cx45.6. Thus, the dissociation between these two proteins that occurs in the mature fibers of late lens development is likely caused by this cleavage. Finally this interaction had no impact on Cx45.6-mediated intercellular communication, suggesting that the Cx45.6-MIP(AQP0) interaction plays a novel unidentified role in lens fibers.


2018 ◽  
Vol 13 (5) ◽  
pp. 536-552 ◽  
Author(s):  
Ankush Ashok Saddhe ◽  
Shweta ◽  
Kareem A. Mosa ◽  
Kundan Kumar ◽  
Manoj Prasad ◽  
...  

2004 ◽  
Vol 279 (30) ◽  
pp. 31813-31822 ◽  
Author(s):  
Nady Golestaneh ◽  
Jianguo Fan ◽  
Robert N. Fariss ◽  
Woo-Kuen Lo ◽  
Peggy S. Zelenka ◽  
...  

2020 ◽  
Author(s):  
Chao Bai ◽  
Yuyan You ◽  
Xuefeng Liu ◽  
Maohua Xia ◽  
Wei Wang ◽  
...  

Abstract Background: Cataracts are defects of the lens that cause progressive visual impairment and ultimately blindness in many vertebrate species. Most cataracts are age-related, but up to one third have an underlying genetic cause. Cataracts are common in captive zoo animals, but it is often unclear whether these are congenital or acquired (age-related) lesions. Results: Here we used a functional candidate gene screening approach to identify mutations associated with cataracts in a captive giant panda (Ailuropoda melanoleuca). We screened 11 genes often associated with human cataracts and identified a novel missense mutation (c.686G>A) in the MIP gene encoding major intrinsic protein. This is expressed in the lens and normally accumulates in the plasma membrane of lens fiber cells, where it plays an important role in fluid transport and cell adhesion. The mutation causes the replacement of serine with asparagine (p.S229N) in the C-terminal tail of the protein, and modeling predicts that the mutation induces conformational changes that may interfere with lens permeability and cell–cell interactions.Conclusion: The c.686G>A mutation was found in a captive giant panda with a unilateral cataract but not in 18 controls from diverse regions in China, suggesting it is most likely a genuine disease-associated mutation rather than a single-nucleotide polymorphism. The mutation could therefore serve as a new genetic marker to predict the risk of congenital cataracts in captive giant pandas.


2006 ◽  
Vol 18 (6) ◽  
pp. 1498-1509 ◽  
Author(s):  
Junpei Takano ◽  
Motoko Wada ◽  
Uwe Ludewig ◽  
Gabriel Schaaf ◽  
Nicolaus von Wirén ◽  
...  

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