Although most OC proteins act as transcriptional activators, at least one example exists in which an OC protein acts to inhibit transcription rather than stimulate it, by antagonizing the activity of another transcription factor (Pierreux 1999). Here we have demonstrated the function of an OC protein like a dose-dependent repressor. that render active or inactive, primarily through transcriptional regulation. DURING development, different RTC-5 concentrations of select dose-dependent signals can induce option cell fates. Among the classes of dose-dependent signals are those that invoke cellCcell communication to determine developmental fate and those that originate and function within the cell to designate fate. In the first class, signaling molecules secreted from one group of cells influence intracellular signaling cascades in neighboring cells. For example, the and woman/hermaphrodite (XX) fate. Both organisms tally the number of X chromosomes relative to the RTC-5 units of autosomes (Madl and Herman 1979), the X:A percentage, using X-linked genes called X signal elements (XSEs) to communicate the X chromosome quantity and autosomal transmission elements (ASEs) to communicate the ploidy. In to induce female development. The solitary dose of XSEs in diploid XY animals (X:A = 0.5) is insufficient to activate is the direct molecular target of the X:A signal and integrates both X and autosomal parts to determine sexual fate. Two copies of XSEs, including the nuclear receptor SEX-1 and the RNA-binding protein FOX-1, induce the hermaphrodite fate in diploid XX embryos by repressing through transcriptional and post-transcriptional mechanisms, respectively (Number 1; Akerib and Meyer 1994; Hodgkin 1994; Nicoll 1997; Carmi 1998). The solitary copy of XSEs in diploid XO embryos cannot overcome activation from the double dose of ASEs, therefore permitting the male fate. One of the ASEs, the T-box transcription element SEA-1 (by increasing its transcript levels (Powell 2005). The X:A signal includes two additional partially characterized parts, Rabbit Polyclonal to C-RAF the XSE (J. Powell, C. Y. Loh and B. Meyer, unpublished results) and the ASE (P. Nix and B. Meyer, unpublished results). Open in a separate window Number 1. The genetic pathway for sex dedication and dose payment in as an XSE and partial analysis of the XSE genes. The SDC proteins result in assembly of the dose compensation complex (SDC-1, SDC-2, SDC-3, DPY-21, DPY-26, DPY-27, DPY-28, DPY-30, Blend-1) on X, where it reduces gene manifestation by half. SDC proteins also promote the hermaphrodite fate by repressing is definitely active, the genes are repressed, advertising the male fate by permitting manifestation and preventing assembly of the dose compensation machinery on X. The genes in boldface type are active in a specific sex. Genes in reddish type are required for hermaphrodite development; genes in blue type are required for male development. The worm sex-determination mechanism discriminates with great accuracy between small variations in the X:A signal. An X:A of 0.67 dictates male fate and an X:A of 0.75 dictates hermaphrodite fate, implying that the effectiveness of the signal might derive from the combined action of multiple X and autosomal elements. Indeed, previous genetic analysis provided RTC-5 evidence that additional X signal elements exist, but did not identify the specific genes (Akerib and Meyer 1994; Carmi and Meyer 1999). Our goal in this study was to identify and characterize fresh XSEs and to further analyze known XSEs to understand the principles by which intracellular signals can induce different developmental fates inside a concentration-dependent manner. Analysis of the X:A signal is complicated by the fact that the transmission controls viability as well as sexual fate. In addition to controlling sex determination, settings X chromosome dose compensation, the vital process that equalizes X-linked gene products between XX and XO animals by halving gene manifestation from both hermaphrodite X chromosomes (examined in Meyer 2005). In XX animals, a decrease in XSE dose or an increase in ASE dose can activate units the male fate by repressing the hermaphrodite-specific genes, which coordinately control downstream genes specialized.