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Today Im going to write about this article I read in a science class. It is not very often that I get to read something that is not philosophy so reading something science related was very interesting. When I was younger I wanted to become a doctor. Then I realized that I hated science and changed my mind. Now I feel like I like science so maybe I made a bad choice. Anyways, in the article, “The opposing homeobox genes Goosecoid and Vent 1/2 self-regulate Xenopus patterning”, researchers attempt to identify how the homeobox genes Goosecoid (Gsc) and Vent 1/2 interact in order to regulate mesodermal and neuroectodermal patterning in Xenopus embryos during gastrulation. Previous experiments by Nierhs et al (1993, 1994) and Steinbeisser et al (1995) involving the modified expression of Gsc have shown that Gsc is needed for promoting dorsalization of mesodermal tissues, and head formation in Xenopus. It is expressed in the dorsal mesoderm, the Spemann organizer. The new technique of using antisense morpholinos (MOs) in loss-of-function experiments prompted researchers to restudy the role of Gsc in this paper. A 1995 research article by Gawantka et al also proposed that Gsc and Vent1/2 repress each other in a cross-regulatory loop, so the function of Vent 1 and 2 were also studied in this paper. Vent 1/2 are induced by BMP4 and are expressed in the ventral mesoderm anlage. They are intrinsic determinants for visceral muscle, the vascular system, and mesodermal patterning on the ventral side of the embryo.
The significance of this question, other than to understand the process and the roles of the homeobox genes, involves a variety of different applications. Firstly, understanding this process can elucidate our understanding of self-regulation mechanisms. Also, it will give us more understanding of the molecular mechanisms of genetic redundancy that are present during embryonic development, to compensate for loss of certain genes. Gsc is also a major mediator of epithelial-mesenchymal transition in tumor metastases of mammals; the opposing interactions between Gsc and Vent 1/2, which affect cell migration in the prechordal plate of the Xenopus embryo and can be used by cancer cells to promote invasiveness, may play a significant part in cancer.
Loss of function and gain of function of the genes were done in the Xenopus model organism. Antisense MO injections were done for loss of function studies, which prevents the successful expression of mRNA’s. Gain of function studies were done via mRNA injection into the embryo. Also, quantitative RT-PCR was used to see how levels of RNA expression were affected by experimental adjustments.
In Figure 1, the importance of Gsc’s role in the patterning of Xenopus embryos is revealed. The injection of a MO, which targeted against both alleles of Gsc, into the vegetal pole of the embryo resulted in severe truncations of the head and ventralization of the embryo. The phenotypes of these embryos affected by MO knockdown of Gsc were completely rescued when mouse Gsc (mGsc) mRNA was co-injected. These results show that Gsc is required for head formation and patterning of the dorsal-ventral axis in developing Xenopus embryos.
Figure 2 illustrates results that show the importance of Chordin (Chd), a downstream target of Gsc. The increased expression of Chd after injecting mGsc mRNA and the decreased expression of Chd in Gsc-depleted embryos confirmed that Chd is in fact a downstream target of Gsc. The researchers also tested whether or not Chd is required for axis induction caused by Gsc. Injection of mGsc mRNA into a ventral blastomere resulted in a range of dorsalized phenotypes. However, injection of mGsc mRNA and Chd MO led to a rescue of normal development in 97% of the embryos. The conclusion of these results is that Chd is needed to mediate the dorsalizing effects of Gsc. This conclusion was further supported when injection of mGsc mRNA induced Chd expression and rescued the dorsal axis in embryos ventralized by UV irradiation, but did not in Chd-depleted embryos. Gsc gain-of-function, therefore, depends on the expression of its downstream target Chd.
The significance of this question, other than to understand the process and the roles of the homeobox genes, involves a variety of different applications. Firstly, understanding this process can elucidate our understanding of self-regulation mechanisms. Also, it will give us more understanding of the molecular mechanisms of genetic redundancy that are present during embryonic development, to compensate for loss of certain genes. Gsc is also a major mediator of epithelial-mesenchymal transition in tumor metastases of mammals; the opposing interactions between Gsc and Vent 1/2, which affect cell migration in the prechordal plate of the Xenopus embryo and can be used by cancer cells to promote invasiveness, may play a significant part in cancer.
Loss of function and gain of function of the genes were done in the Xenopus model organism. Antisense MO injections were done for loss of function studies, which prevents the successful expression of mRNA’s. Gain of function studies were done via mRNA injection into the embryo. Also, quantitative RT-PCR was used to see how levels of RNA expression were affected by experimental adjustments.
In Figure 1, the importance of Gsc’s role in the patterning of Xenopus embryos is revealed. The injection of a MO, which targeted against both alleles of Gsc, into the vegetal pole of the embryo resulted in severe truncations of the head and ventralization of the embryo. The phenotypes of these embryos affected by MO knockdown of Gsc were completely rescued when mouse Gsc (mGsc) mRNA was co-injected. These results show that Gsc is required for head formation and patterning of the dorsal-ventral axis in developing Xenopus embryos.
Figure 2 illustrates results that show the importance of Chordin (Chd), a downstream target of Gsc. The increased expression of Chd after injecting mGsc mRNA and the decreased expression of Chd in Gsc-depleted embryos confirmed that Chd is in fact a downstream target of Gsc. The researchers also tested whether or not Chd is required for axis induction caused by Gsc. Injection of mGsc mRNA into a ventral blastomere resulted in a range of dorsalized phenotypes. However, injection of mGsc mRNA and Chd MO led to a rescue of normal development in 97% of the embryos. The conclusion of these results is that Chd is needed to mediate the dorsalizing effects of Gsc. This conclusion was further supported when injection of mGsc mRNA induced Chd expression and rescued the dorsal axis in embryos ventralized by UV irradiation, but did not in Chd-depleted embryos. Gsc gain-of-function, therefore, depends on the expression of its downstream target Chd.
