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:
Answer:
A
Explanation:
zygote is the merged gametes of different organisms
Answer:
B) a nonsense mutation; this is because a nonsense mutation results in the change of a regular amino acid codon into a stop codon, which ceases translation. This fits with the problem's description of the protein that causes the symptoms as too short, as translation is the process by which proteins/polypeptides are created. A missense mutation would not be the answer because it still codes for an amino acid, which would not shorten the protein. A duplication of the gene would probably just lengthen the protein or not affect its length at all.
Answer:
have curved protofilaments at their plus ends
Explanation:
Microtubules are polymers of tubulin proteins that function as the cytoskeleton of eukaryotic cells. Microtubules are dynamic structures that can grow and shrink at a rapid rate. During this process, tubulin subunits can associate and dissociate at the plus end of the protofilament. Tubulin subunits bind to two GTP molecules, one of which is hydrolyzed to GDP after assembly. When microtubules are unstable, protofilaments curl outwards because GDP-bound tubulin has a weak affinity (thereby curving it) and disassemble. The dynamic stability of microtubules is regulated by a feedback loop: when microtubules shrink, free tubulin concentration increases and microtubules start to grow. As microtubules grow, free tubulin concentration decreases and the rate of GTP-tubulin addition also decreases.
The answer would be a. Energy stored in chemical bonds :)
