For Figure 2: Why are they doing the experiment? What is the hypothesis that the
ID: 202959 • Letter: F
Question
For Figure 2:
Why are they doing the experiment? What is the hypothesis that they are testing?
How did they do it? Describe the technique(s) used to obtain the results shown in this figure.
What did they find? Describe the results along with the controls.
So what? What are the conclusions of the data shown in this figure?
Figure 2. A sea-1 Mutation Permits the Dos- age Compensation Complex to Assemble onto th@ Chromosomes of for-1er. 1 XX Mutant Embryos Confocal images of mutant or wild-type xx embryos at approximately the 100-cel stage, costained with antibodies against the dosage compensation proteins DP-27 green) and SDC-3 (red) and with DAPI bluel, a DNA-inter- calating dye A) In wild-type Xx embryos, DPY-27 and SDC-3 localze specifically to X chromo- fox-1 sex-1 sea-1; fox-1 sex-1 9 B) In fox-sex- mutant embryos, the dos- age compensation complex cannot assem- ble on X, causing XX animas to die from overexpression of X-inked genes. In these mutants, SDC-3 is absent and DPY-27 is greatly reduced in abundance. Residual DPY-27 is diffusely distributed within nuclei (C) sea-1y356) suppresses fox-1 sex-1 e- thality by restoring the levels of dosage com- pensation proteins and permitting assembly of the complex onto hermaphrodite X chro- mosomes. Scale bars equal 5 um 2 transcription of xol-, thereby inducing male develop-eny that inherit this mitotically unstable array survive ment. Hence, xol-1 integrates both X and autosomal (green), while progeny that fail to inherit the array die signals to determine sexual fate. (non-green) (Figure 1C). We sought mutations that per- mitted fox-1 sex-1 hermaphrodites to live without the array (non-green). These suppressor mutations are can- didate ase(f mutations. In principle, many classes of mutations could be re- Genetic Screen for Autosomal Signal Elements To isolate loss-of-function mutations in potential ASE covered from this screen: loss-of-function (If) mutations genes, we designed a sensitized genetic screen that in ASEs or in xol-1 and gain-of-function (gf mutations took advantage of the synergistic behavior of X chro- in XSEs. Among the suppressors isolated were one xol- mosome signal elements (Figure 1C). Although XX ani 1(f allele and the allele y356, a loss-of-function muta- mals carrying a null mutation in the XSE fox-1 have no o shown below to disrupt an autosomal signal el- tation in the XSE sex-1 have only reduced viability, all xx animals homozygous for both null mutations, fox- 1y303) and sex-1y263), die from the failure to asseCriteria for an Autosomal Signal Element ble the dosage compensation complex on X (Figures Autosomal signal elements would counter the Xsignal, 2A and 2B; Carmi et al., 1998; Nicoll et al., 1997). Weallowing us to predict the consequences of changing reasoned that disruption of an ASE gene, even one with the dose of a candidate ASE gene. Loss-of-function a small contribution to the autosomal signal, would mutations in an ASE gene help restore the XA balance and hence suppress the hality caused by loss-of-function mutations in XSE XX lethality, at least in part (Figure 1B). suppress the XX le- genes and enhance the XO lethality caused by increas- For the screen, fox-1 sex-1 doubly mutant hermaph- ing XSE dose. Conversely, increasing ASE dose should rodites were maintained as a viable strain by a trans enhance the XX lethality from XSE loss-of-function mu- genic array that ectopically expresses sdc-2 from the tations and suppress the XO lethality from increasing non-sex-specific promoter dpy-30. SDC-2 produced XSE dose. An ASE must act in a dose-dependent man- from yEx483[Pdpy-30:sdc-21+ induces assembly of ner in the zygote, because the zygotic XA signal deter- the dosage compensation complex on X chromosomes mines sex. As shown below, the gene defined by the independent of either the XA signal or level of xol- ox-1 sex-1 suppressor mutation y356 meets these cri- expression (Dawes et al., 1999). The array also caries teria, and moreover, it controls sex determination as the myo-2:gfp transformation marker, which causes well as dosage compensation. We named the gene the pharynx to be green. The 55% of fox-1 sex-1 prog- sea-1 (signal element on an autosome).Explanation / Answer
1. Hypothesis
Autosomal signal elements genes affect the survival effect by regulating the X chromosome signal elements.
They are trying to get the assembly of dosage compensation complex in a double mutant fox1 ans sex 1 mutant embryo.
2. Techniques used
Gene knockout
Fluroscent microscope
They are targeting specific gene to know out the gene function fox1, sex1 and sea1 genes. Then seeing the effect
with diffrent experiment by adding respective fluroscence compounds to for result.
3.The control is wild type embryo they are not undergo any mutation or knockout.
Wildtype all are normal function. Ib fox1 and sex1 mutation both null mutation brings the embryo lethal. It shown in SDC3 not assemble in Image B. But if we further mutate in sea1 gene the embryo survive shown in fig C.
4. They find that Loss of function mutation in an ASE gene suppress the XX lethality caused by loss of function by mutation in XSE gene fox1 and sex1 gene.
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