) Figure 1: The authors perform a genetic screen in which they mutagenize a stra
ID: 202958 • Letter: #
Question
) Figure 1: The authors perform a genetic screen in which they mutagenize a strain carrying loss-of-function mutations in fox-1 and sex-1 and that has an "extrachromosomal array" which has a transgene that drives ectopic expression of sdc-2, using the non-sex-specific promoter, dpy-30. Note: "extrachromosomal" arrays in worms are not transmitted to progeny in a reliable way as chromosomes are. Therefore, they are only transmitted to a fraction of the progeny in a random (non-Mendelian) distribution. That is, worms that carry an extrachromosomal array will have progeny that contain the array (green pharynx) and progeny that do not contain the array (not green pharynx). Question: Why do fox-1; sex-1 double mutants die and why does ectopic sdc-2 expression in fox-1;sex-1 double mutants allow these double mutants to survive?
tosomal signal could be an indirect reflection of chro- mosome number, which changes with ploidy. For exam- ple, as chromosome number increases, so does the concentration of nonspecific DNA sites that might bind XSEs with low affinity. An increase in such sites would reduce XSE binding to bona fide target sites within xol-1 thereby disrupting repression of xol-1. Alternatively, the autosomal signal might act more specifically to counter XSEs, but be composed of discrete elements that act in cis, unlike XSEs, which act in trans. For example, the 2X:2A osdc-2-Ofate binding sites for XSEs, which would titrate XSEs away from their xol-1 targets, thereby activating xol-1 Like the X signal, the autosomal signal could regulate the master sex switch gene xol-1, the target of XSEs. XSEs ASEs Wild type tion and dosage compensation pathway might interpret the autosomal signal (Figure 1A). The autosomal signal might act like the X signal to coordinately control both XSEs ASEs XSEs & ASES XSEs&TASEs; Dead-Dpy -Masc Suppressed Enhanced lating a single target gene that directs both processes, or it might act instead on more specialized targets to Our work reveals the genetic and molecular character of the autosomal signal in C. elegans sex determina- tion. The autosomal signal includes discrete, trans-act- ing ASEs that counter XSEs to coordinately control XSEs & TASEs XSEs&ASEs Suppressed Enhanced the first ASE identified in C. elegans, encodes a T-box B) Predicted outcomes from changing the dose of X and autoso- mal signal elements in 2X2A and 1X:2A animals. Mutations in X xX animals with ase mutations die from the disruption of doeage compensation, and the survivors are masculinized and dumpy Dpy) Mutations in potential autasomal signal elements (ASE) ones apposite to those caused by XSE mutations. Moreover, since the sex determination signal is the ratio of X chromosomes to au tasomes, a decrease in the dose of ASEs in XX animals is predicted to compensate for a decrease in the dase of XSEs by restoring the overall balance of the perceived X:A signal. Conversely, an increase in the dose ASEs in XO animals shoukd compensate for an increase in XSEs. Furthermore, an increase in the dose o ASEs in XX ani mals should enhance the mutant phenotype caused by a decrease in XSEs, and a decrease in the dose of ASEs in XO animals should enhance the mutant phenotype caused by an increase in XSEs. In the figure, a decrease in the dose of either XSEs or ASEs is repre- sented by a downward arrow, and an increase in XSE or ASE dose is represented by an upward anow. If the change in signal element dose is masculinizing, the arrow is aqua; it the change is feminizing fox-1 sex-1 fox-1 sex-1 fox-1 sex-1 Figure 1. Identification and Characterization of the Autosomal Component of the C. elegans X:A Sex Determination Signal A) Genetic hierarchy regulating sex determination and dosage compensation. The ratio of X chromosomes to sets of autosomes is the primary signal that determines sexual fate and the level of x chromosome gene expression. In xX diploids (2X:2A), xol is repressed, permitting high expression ot sdc-2, the pivotal XX-spe- cific trigger of dosage compensation and hermaphrod te develop- ment. In XO diploids (1X:2A) xoi-1 is active and sdc-2 is repressed, (C) Genetic screen for mutations in ASE genes. The viability ot her- maphrodites doubly mutant for the XSEs fox-T sex-1 depends on pressing xo-1 when they are present in two doses but not in one dose. The autosomal signal must appose the X signal, but prior to our current work, the nature of the autosomal signal was nat known. A key question was whether a group of discrete, dose sensitive autosomal signal elements (ASEs) communicates autoso- mal dose in a manner analogous to XSEs. somal array that averexpresses sdc-2f) constitutively from a pro- moter insensitive to the XA signa This aray, referred to as yExfsdc-2fin the figure, also carries the marker myo-2.gfp, which causes the pharyrx to be green. Folowing mutagenesis with EMS, mutations that suppress fox-1 sex-1 lethality can be recov ered from hermaphrodites that acquire the ablity to live in the ab- sence of the rescuing array and therefore do not have a green phar- These are candidate loss-of-function mutations in ASEs.Explanation / Answer
Animals with XX shifting a null mutation in the X Signal Elements (XES) fox-1 have no pronounced phenotype and animals with XX shifting a null mutation in the XSE sex-1 have decreased feasibility only, each animals with XX homozygous mutants for both, fox-1 and sex-1, do not survive due to the non success to collect the complex of dosage compensation on X. Cause given that interference of an autosomal signal elements (ASE) gene, similarly one with a less allowance to the autosomal signal, would support establish the balance between X:A and therefore repress the lethality of XX, at least in some portion.
SDC-2 generated from yEx483[Pdpy-30::sdc-2(+)] initiates convocation of the dosage compensation complex on chromosome X unconventional to either the X:A signal or xol-1 expression level.
Related Questions
Navigate
Integrity-first tutoring: explanations and feedback only — we do not complete graded work. Learn more.