Nuclear cataract caused by a lack of DNA degradation in the mouse eye lens

Sogo Nishimoto, Kohki Kawane, Rie Watanabe-Fukunaga, Hidehiro Fukuyama, Yoshiyuki Ohsawa, Yasuo Uchiyama, Noriyasu Hashida, Nobuyuki Ohguro, Yasuo Tano, Takeshi Morimoto, Yutaka Fukuda and Shigekazu Nagata ()
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Sogo Nishimoto: Department of Genetics
Kohki Kawane: Department of Genetics
Rie Watanabe-Fukunaga: Department of Genetics
Hidehiro Fukuyama: Department of Genetics
Yoshiyuki Ohsawa: Department of Cell Biology and Neuroscience
Yasuo Uchiyama: Department of Cell Biology and Neuroscience
Noriyasu Hashida: Graduate School of Frontier Biosciences, Osaka University
Nobuyuki Ohguro: Department of Ophthalmology
Yasuo Tano: Department of Ophthalmology
Takeshi Morimoto: Osaka University Medical School
Yutaka Fukuda: Osaka University Medical School
Shigekazu Nagata: Department of Genetics

Nature, 2003, vol. 424, issue 6952, 1071-1074

Abstract: Abstract The eye lens is composed of fibre cells, which develop from the epithelial cells on the anterior surface of the lens1,2,3. Differentiation into a lens fibre cell is accompanied by changes in cell shape, the expression of crystallins4 and the degradation of cellular organelles5,6. The loss of organelles is believed to ensure the transparency of the lens, but the molecular mechanism behind this process is not known. Here we show that DLAD (‘DNase II-like acid DNase’7, also called DNase IIβ8) is expressed in human and murine lens cells, and that mice deficient in the DLAD gene are incapable of degrading DNA during lens cell differentiation—the undigested DNA accumulates in the fibre cells. The DLAD-/- mice develop cataracts of the nucleus lentis, and their response to light on electroretinograms is severely reduced. These results indicate that DLAD is responsible for the degradation of nuclear DNA during lens cell differentiation, and that if DNA is left undigested in the lens, it causes cataracts of the nucleus lentis, blocking the light path.

Date: 2003
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DOI: 10.1038/nature01895

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