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研究生:蔡玉真
研究生(外文):Yu-Chen Tsai
論文名稱:unpaired基因調控果蠅眼睛發育之研究
論文名稱(外文):Functional analysis of the unpaired gene in Drosophila eye
指導教授:孫以瀚孫以瀚引用關係
指導教授(外文):Y. Henry Sun
學位類別:博士
校院名稱:國立陽明大學
系所名稱:遺傳學研究所
學門:生命科學學門
學類:生物訊息學類
論文種類:學術論文
論文出版年:2004
畢業學年度:92
語文別:英文
論文頁數:107
中文關鍵詞:果蠅眼睛發育unpaired 基因
外文關鍵詞:unpairedJak/STAT pathwayDrosophilaeye development
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中文摘要
unpaired (upd)基因表達一種細胞外的蛋白質, 調控果蠅中Jak/STAT 訊號傳
息傳遞鏈. 它表達在二齡幼蟲及三齡幼蟲的眼碟後端的中點. upd 會影響到眼睛
大小的發育. 大量表達 Upd 蛋白, 會使複眼變大. 它的突變株, 成蟲複眼會變
小為正常果蠅的一半. 我的研究發現, Upd 透過下游Dome/Jak/STAT 促進細胞增
生, 進而影響眼睛大小.
Upd 蛋白作用在眼碟凹溝前端未分化的細胞, 但是眼碟凹溝後方正在分化
的細胞不受它影響. Upd 蛋白會影響非自主性的細胞增生. 影響細胞分裂週期重
要基因 cyclin D (cycD), 在眼碟凹溝前端會受到 upd 基因的調控. 細胞外Upd
蛋白可被偵測遠達眼碟凹溝前端20 個細胞的範圍, 這與其作用的距離相當. Upd
是一個可以遠距離作用的訊息調控分子.
Notch (N)和eyegone (eyg) 基因在複眼發育過程中, 對細胞增生的調控伴演
重要角色. 我的研究發現, N 和 eyg 突變與upd 突變有加成作用. 在eyg1突變中
upd-lacZ 在眼碟的表達消失. 不論表達eyg 或N 都能誘導 upd 基因的表達. 而
且表達upd可以補償 eyg 突變株或表達 NDN 造成小眼的缺陷. 由這些結果顯示,
upd 是在N 及eyg 基因的下游, 透過調控眼睛細胞的增生影響眼睛的大小.
upd 表達在眼碟凹溝開始的起點, 它在眼碟兩側會正向調控 dpp 基因的表
現--這個與眼碟凹溝開始分化所必需的基因. 它也會抑制拮抗影響眼碟凹溝開始
分化的 wingless 基因表達. 表達upd 在眼盤背面側邊可以誘導產生一個新的複
眼產生. 這顯示 upd 除了調控細胞增生外, 也影響眼睛形態的生成.
ABSTRACT
unpaired (upd) encodes a ligand for the Jak/STAT signaling pathway in
Drosophila. In the second instar and early third larval eye disc, upd is expressed in the
center of the posterior margin. upd loss-of-function mutations caused eye size
reduction and upd over-expression caused eye enlargement. Upd regulates eye size
through the Dome/Jak (Hop)/STAT92 signaling pathway to promote cell proliferation.
Interestingly the effect of Upd is only on cells located anterior to MF, but has no
effect on the second mitotic wave, which is posterior to MF. Overexpression of upd
behind MF can non-autonomously induce cell proliferation in the anterior region. The
G1 cyclin, cycD transcript level was also enhanced anterior to MF. Consistent with the
long-range effect, I found that the extracellular Upd protein can be detected over a
comparable long range up to 20 rows of cells anterior to MF, suggesting that Upd acts
directly over a long distance as a signaling molecule.
N and eyg regulate in the cell proliferation during eye development. I found that
N and eyg have genetic interaction with upd. Either N or eyg can induce upd
expression. Overexpression of upd can rescue the defect caused by eyg mutant or ey>
NDN. These suggest that upd is downstream to N and eyg to regulate eye development.
In the early 3rd instar, upd is expressed in the furrow initiation site of the eye disc.
Ectopic expression of upd at lateral margins can induce dpp expression which is
required for furrow initiation, and repress wg expression which antagonizes furrow
initiation. At dorsal lateral margin, expression of upd can induce ectopic eye field.
These indicate that upd can regulate pattern formation during eye development
besides its function on promoting cell proliferation.
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