Sellin Julia, Drechsler Maik, Nguyen Hanh T, Paululat Achim
Universität Osnabrück, Fachbereich Biologie/Chemie - Zoologie/Entwicklungsbiologie, Osnabrück, Germany.
Dev Biol. 2009 Feb 15;326(2):444-55. doi: 10.1016/j.ydbio.2008.10.041. Epub 2008 Nov 11.
In this study we show that cell fate decisions in the dorsal and lateral mesoderm of Drosophila melanogaster depend on the antagonistic action of the Gli-like transcription factor Lame duck (Lmd) and the zinc finger homeodomain factor Zfh1. Lmd expression leads to the reduction of Zfh1 positive cell types, thereby restricting the number of Odd-skipped (Odd) positive and Tinman (Tin) positive pericardial cells in the dorsal mesoderm. In more lateral regions, ectopic activation of Zfh1 or loss of Lmd leads to an excess of adult muscle precursor (AMP) like cells. We also observed that Lmd is co-expressed with Tin in the early dorsal mesoderm and leads to a reduction of Tin expression in cells destined to become dorsal fusion competent myoblasts (FCMs). In the absence of Lmd function, these cells remain Tin positive and develop as Tin positive pericardial cells although they do not express Zfh1. We show further that Tin repression and pericardial restriction in the dorsal mesoderm facilitated by Lmd is instructed by a late Decapentaplegic (Dpp) signal that is abolished in embryos carrying the disk region mutation dpp(d6).
在本研究中，我们表明果蝇背侧和外侧中胚层中的细胞命运决定取决于类Gli转录因子跛脚鸭（Lmd）和锌指同源域因子Zfh1的拮抗作用。Lmd的表达导致Zfh1阳性细胞类型减少，从而限制了背侧中胚层中奇跳（Odd）阳性和锡人（Tin）阳性心包细胞的数量。在更外侧区域，Zfh1的异位激活或Lmd的缺失导致出现过量的成体肌肉前体细胞（AMP）样细胞。我们还观察到，Lmd在早期背侧中胚层中与Tin共表达，并导致注定成为背侧融合能力成肌细胞（FCM）的细胞中Tin表达减少。在缺乏Lmd功能的情况下，这些细胞保持Tin阳性，并发育为Tin阳性心包细胞，尽管它们不表达Zfh1。我们进一步表明，Lmd促进的背侧中胚层中Tin的抑制和心包限制是由晚期的骨形态发生蛋白（Dpp）信号指导的，该信号在携带盘区突变dpp（d6）的胚胎中被消除。
