Answer:
The C. elegans embryo is a powerful model system for studying the mechanics of metazoan cell division. Its primary advantage is that the architecture of the syncytial gonad makes it possible to use RNAi to generate oocytes whose cytoplasm is reproducibly (typically >95%) depleted of targeted essential gene products via a process that does not depend exclusively on intrinsic protein turnover. The depleted oocytes can then be analyzed as they attempt their first mitotic division following fertilization. Here we outline the characteristics that contribute to the usefulness of the C. elegans embryo for cell division studies. We provide a timeline for the first embryonic mitosis and highlight some of its key features. We also summarize some of the recent discoveries made using this system, particularly in the areas of nuclear envelope assembly/ dissassembly, centrosome dynamics, formation of the mitotic spindle, kinetochore assembly, chromosome segregation, and cytokinesis.
1. The C. elegans embryo as a system to study cell division
The C. elegans embryo is a powerful model system for studying the mechanics of metazoan cell division. Its primary advantage is that the syncytial gonad makes it possible to use RNA interference (RNAi) to generate oocytes whose cytoplasm is reproducibly (>95%) depleted of targeted essential gene products. Introduction of dsRNA rapidly catalyzes the destruction of the corresponding mRNA in many different systems. However, depletion of pre-existing protein is generally a slow process that depends on the half-life of the targeted protein. In contrast, in the C. elegans gonad, the protein present when the dsRNA is introduced is depleted by the continual packaging of maternal cytoplasm into oocytes (Figure 1). Since depletion relies on the rate of embryo production instead of protein half-life, the kinetics tend to be similar for different targets. By 36-48 hours after introduction of the dsRNA, newly formed oocytes are typically >95% depleted of the target protein.
Explanation:
Cells are very different but have similar properties
Researchers have identified specific gene variants in the receptors that detect sweetness: TAS1R2 and TAS1R3. There is also high variation in the detection of bitterness. However, the story is more complicated than sweet taste, as we have 25 receptors that detect different bitter molecules
Answer:
The correct answer is 4: "The exception to Mendelian laws of inheritance that best explains the mentioned symptoms is codominance".
Explanation:
In codominance, both alleles can be expressed. In these cases, heterozygote individuals<em> instead</em> of showing an <em>intermediate phenotype</em>, express both of the alleles. Their phenotype is an additive expression of their parents' genes.
In cystic fibrosis, there is a gene responsible for coding for a protein named "cystic fibrosis transmembrane conductance regulator, CFTR".
-Most of the people have two copies of the normal allele and produce the functional CFTR protein form.
-Patients with cystic fibrosis have two copies of the mutated allele and so produce the mutated and dysfunctional form for this protein.
-Heterozygote people possess only one normal CFTR allele and a mutated form for the same allele and produce a normal protein and a mutated protein.
In the last case, both alleles are codominant and they express in heterozygote individuals. Given the fact that the normal allele produces enough functional CFTR protein, these individuals do not have any adverse effect and the mutated allele is recessive at a physiological level.
