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Direct interaction of geminin and Six3 in eye development
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Journal Article
Direct interaction of geminin and Six3 in eye development
2004
Overview
Organogenesis in vertebrates requires the tight control of cell proliferation and differentiation. The homeobox-containing transcription factor Six3 plays a pivotal role
1
,
2
in the proliferation of retinal precursor cells. In a yeast two-hybrid screen, we identified the DNA replication-inhibitor geminin as a partner of Six3. Geminin inhibits cell-cycle progression
3
by sequestering Cdt1 (refs
4
,
5
), the key component for the assembly of the pre-replication complex
6
. Here, we show that Six3 efficiently competes with Cdt1 directly to bind to geminin, which reveals how Six3 can promote cell proliferation without transcription. In common with
Six3
inactivation
2
,
7
, overexpression of the geminin gene (
Gem
; also known as
Gmn
) in medaka (
Oryzias latipes
) induces specific forebrain and eye defects that are rescued by
Six3
. Conversely, loss of
Gem
(in common with gain of
Six3
(ref.
1
)) promotes retinal precursor-cell proliferation and results in expanded optic vesicles, markedly potentiating
Six3
gain-of-function phenotypes. Our data indicate that the transcription factor Six3 and the replication-initiation inhibitor geminin act antagonistically to control the balance between proliferation and differentiation during early vertebrate eye development.
Publisher
Nature Publishing Group UK,Nature Publishing,Nature Publishing Group
Subject
/ Biological and medical sciences
/ Cell Cycle Proteins - genetics
/ Cell Cycle Proteins - metabolism
/ Cells
/ Eye
/ Fundamental and applied biological sciences. Psychology
/ Geminin
/ Genes
/ Homeodomain Proteins - genetics
/ Homeodomain Proteins - metabolism
/ Humanities and Social Sciences
/ Humans
/ letter
/ Nerve Tissue Proteins - genetics
/ Nerve Tissue Proteins - metabolism
/ Science
/ Two-Hybrid System Techniques
/ Vertebrates: nervous system and sense organs
/ Yeasts
