Evidence that sisterless-a and sisterless-b are two of several discrete "numerator elements" of the X/A sex determination signal in Drosophila that switch Sxl between two alternative stable expression states.
Evidence that sisterless-a and sisterless-b are two of several discrete "numerator elements" of the X/A sex determination signal in Drosophila that switch Sxl between two alternative stable expression states.
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有证据表明，sisterless-a 和sisterless-b 是果蝇X/A 性别决定信号的几个离散“分子元件”中的两个，可在两种替代稳定表达状态之间切换Sxl。
DOI：
10.1093/genetics/119.4.829
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发表时间：
1988
期刊：
影响因子：
3.3
通讯作者：
Cline,TW
中科院分区：
文献类型：
--
作者：
Cline,TW
果蝇性别决定的主要信号是X染色体的数量与常染色体的数量的相对关系。本报告表明，该X/A信号的分子似乎是由数量相对有限的离散X连锁遗传元件的累积剂量决定的，其中两个是无姐妹a和无姐妹b。这一关于性别决定信号性质的发现源于先前对可能的X/A信号靶点（雌性化开关基因，Sex-lethal）和该靶基因的两个正调控因子（sis-a和daughterless）的研究。这三个基因的遗传扰动组合已被证明具有协同效应。一个模型提出的部分占这些相互作用产生了大量的各种强有力的预测性别特异性的协同作用，这将是诊断X/A分子元素，并可以区分它们的性别决定系统的其他组件。所有这些预测，以及X/A分子元素的其他预测，在这里都被证明是符合的。最引人注目的观察涉及野生型基因重复的性相互生存力效应：Sis-a+、Sis-b+和/或Sxl+重复的组合对雄性是致命的，但拯救雌性免受性别决定机制其他组分变化的致命影响。这里描述的许多相互作用说明了一个似乎违反直觉的重要原则：果蝇性别决定信号的扰动通常不会影响成年性表型。这一原理来自Sxl参与剂量补偿以及性别决定的事实，以及来自X/A信号和Sxl自身产物（正性自动调节）对Sxl的调节的性质和时间的重要方面。这些因素通过引起细胞和/或个体的过早死亡来掩盖对成体性分化的潜在影响。这里呈现的大量结果符合这一原理的事实是支持X/A信号对Sxl调节的“二元状态”模型的有力证据。该模型优于其他人在X/A信号的不同研究中提出的另一种“多状态”假设。在同一项研究中得出结论，X染色体的3E 8 - 4F 11区域含有特别有效的X/A分子元件。（400字处截断摘要）
The primary signal for Drosophila sex determination is the number of X chromosomes relative to the number of sets of autosomes. The present report shows that the numerator of this X/A signal appears to be determined by the cumulative dose of a relatively limited number of discrete X-linked genetic elements, two of which are sisterless-a and sisterless-b. This discovery regarding the nature of the sex determination signal grew out of previous studies of both the likely X/A signal target (the feminizing switch gene, Sex-lethal) and two positive regulators of that target gene (sis-a and daughterless). Combinations of genetic perturbations in these three genes had been shown to have synergistic effects. A model proposed in part to account for these interactions generated a large variety of strong predictions for sex-specific synergistic interactions that would be diagnostic for X/A numerator elements and could distinguish them from other components of the sex determination system. All these predictions, as well as other predictions for X/A numerator elements, are shown here to be fulfilled. The most compelling observations involve sexually reciprocal viability effects of duplications of wild-type genes: combinations of sis-a+, sis-b+ and/or Sxl+ duplications are lethal to males but rescue females from the otherwise lethal effects of changes in other components of the sex determination machinery. The many interactions described here illustrate an important principle that may seem counter-intuitive: perturbations of the sex determination signal for Drosophila generally will not appear to affect adult sexual phenotype. This principle follows from the fact that Sxl is involved in dosage compensation as well as sex determination, and from important aspects of the nature and timing of Sxl's regulation both by the X/A signal and by Sxl's own products (positive autoregulation). These factors mask potential effects on adult sexual differentiation by causing the premature death of cells and/or individuals. The fact that the vast array of results presented here conform to this principle is strong evidence in favor of a "binary state" model for Sxl regulation by the X/A signal. This model is favored over an alternative "multiple state" hypothesis that was proposed by others in a different study of the X/A signal. In that same study it was concluded that region 3E8-4F11 of the X chromosome contained especially potent X/A numerator elements.(ABSTRACT TRUNCATED AT 400 WORDS)