QUESTION 37 Which describes the cell's cortex? O the region of cytoplasm just inside the plasma membrane that is rich in actin, actin-binding proteins and myosins O the nucleoplasm just inside the nuclear envelope that is rich in nuclear lamins the proteins around the centriole, including gamma-tubulin ring complexes O the region around the MTOC where it is closely associated with the trans face of the Golgi apparatus
Q: The known information pertinent to the organelles found in bacterial cells Question 35 options:…
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Q: motor protein(s) that can carry vesicles along microtubules?
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A: CDK are the protein kinase which are involved in the regulation of cell cycle.
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Q: QUESTION 48 Condensed chromatin: O a. chromosomes O b: cytoplasm C. cytosol O d. amorphic organelles
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Proteins
We generally tend to think of proteins only from a dietary lens, as a component of what we eat. However, they are among the most important and abundant organic macromolecules in the human body, with diverse structures and functions. Every cell contains thousands and thousands of proteins, each with specific functions. Some help in the formation of cellular membrane or walls, some help the cell to move, others act as messages or signals and flow seamlessly from one cell to another, carrying information.
Protein Expression
The method by which living organisms synthesize proteins and further modify and regulate them is called protein expression. Protein expression plays a significant role in several types of research and is highly utilized in molecular biology, biochemistry, and protein research laboratories.
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- APOE gene has been found to be a major contributor to sporadic Alzheimer's disease (AD), by acting as an age-of-onset modifier for the common relatively late-onset forms of the disease. Among four alleles causing early onset of AD, the epsilon4 allele (APOE4) disrupts this function. If you generate transgenic monkeys in which the normal allele of APOE gene is knocked out, what phenotype will you expect for those knockout monkeys? A. The APE mRNA expression will be completely suppressed. B. They slow down the development of AD. C. They develop AD early. D. They don't show any AD symptom.Suppose you have six strains of E. coli. One is wildtype, and each of the other five has a single one of thefollowing mutations: lacZ−, lacY−, lacI−, oc, andlacIS. For each of these six strains, describe thephenotype you would observe using the following assays. [Notes: (1) IPTG is a colorless synthetic molecule that acts as an inducer of lac operon expressionbut cannot serve as a carbon source for bacterialgrowth because it cannot be cleaved byβ-galactosidase; (2) X-gal cannot serve as a carbonsource for growth; (3) E. coli requires active lactosepermease (the product of lacY) to allow lactose,X-gal, or IPTG into the cells.] Colony color in medium containing glycerol as theonly carbon source and X-gal, but no IPTG.d. Colony color in medium containing high levels ofglucose as the only carbon source, X-gal, andIPTG.e. Colony color in medium containing high levels ofglucose as the only carbon source and X-gal, butno IPTG. Suppose you have six strains of E. coli. One is wildtype, and each of the other five has a single one of thefollowing mutations: lacZ−, lacY−, lacI−, oc, andlacIS. For each of these six strains, describe thephenotype you would observe using the following assays. [Notes: (1) IPTG is a colorless synthetic molecule that acts as an inducer of lac operon expressionbut cannot serve as a carbon source for bacterialgrowth because it cannot be cleaved byβ-galactosidase; (2) X-gal cannot serve as a carbonsource for growth; (3) E. coli requires active lactosepermease (the product of lacY) to allow lactose,X-gal, or IPTG into the cells.]a. Growth on medium in which the only carbonsource was lactose.b. Colony color in medium containing glycerol as theonly carbon source, X-gal, and IPTG
- this is what i have said about this image so far, what else can be said aswell including the raw count column. " Interpreting the results of an RNA-Seq analysis is pivotal in understanding the underlying genetic mechanisms of diseases such as breast cancer. In this analysis, Figure 1 provides comprehensive data on differentially expressed genes associated with breast cancer. By delving into the provided information, we can gain valuable insights into the molecular landscape of this disease. First focus is on the gene with the highest fold change, EYA4, situated on chromosome 6. With a staggering fold change of 3604.4176, EYA4 exhibits an unprecedented level of overexpression in cancerous cells compared to normal cells. This profound alteration suggests a pivotal role for EYA4 in breast cancer pathogenesis. The log2 fold change of 11.81555 further emphasizes the magnitude of this difference in gene expression. Statistical significance is evident, with an exceptionally low p-value of…Below is a figure (here called Figure 1) from “Prognostic Significance of CpG Island Methylator Phenotype and Microsatellite Instability in Gastric Carcinoma,” by An et al., published in Clinical Cancer Research in 2005. The authors look at five microsatellite loci (BAT 25, BAT 26, D2S123, D5S346, and D17S250) in normal (N) and tumor (T) tissue from patients with Gastric Carcinoma. They amplify the loci by PCR and then instead of using standard agarose gel electrophoresis, they run the PCR products through capillary gel electrophoresis and detect bands as they pass a laser near the positive charge terminal. The x-axis in these plots is the time at which the band passed the laser (aka size of the PCR product) and the intensity of the peaks represents the amount of DNA in that band A. Which patient- 18, 30, or 1- shows the most microsatellite instability? Which patient shows the least? How do you know? B. In which repair pathway is it most likely that you will find the driver mutations…Gal4–VP16 requires SAGA for activation. Strains containing the Gal4+, Gal4–VP16, or Gal4–VP16–F442A activators were tested for their ability to grow on glucose and galactose as carbon sources and for their dependence on Spt20 for activation. Strains were tested for growth on SC-Leu plates containing glucose or galactose by replica plating and are shown after 4 d of growth at 30°C. The SPT20 allele and the activator present in each strain is shown in the figure. a) Describe the strain Spt20+Gal4Δ (Fig. 5B above). Is this strain able to activate the Gal genes? Why or why not? b) What is VP16-FA? please answer this fully, this is my second time posting the first time it was answered incorrectly THIS IS THE COMPLETE QUESTION
- Assume that there is a double stranded break on DNA double helix of an eukaryotic cell due to X-ray radiation and it is not repaired. In addition, the cell’s Apaf-1 protein is not expressed due to a null mutation in the Apaf-1 gene. Please discuss the effect of not having Apaf-1 expression in the cell with non-repaired double stranded break.A research group is studying a bacterium X that binds to mucosal cells in the lung and invades. Wildtype X has an LD50 value of 10 bacteria when administered to mice by inhalation. Using transposon mutagenesis, the researchers have isolated two mutants of X that they call Xmut1 and Xmut2, both of which have LD50 values of 105 when inhaled by mice. However, in tissue culture cells, Xmut1 can invade the cells just as well as wild-type X, while Xmut2 cannot. Provide a possible explanation for these results.A wild-type mouse that is heterozygous for two immunoglobulin heavy chain alleles (IgHa/b) generates the population of B cells shown on the left of the figure below. A mouse strain, also IgHa/b, carries an inactivating mutation in the VpreB gene. In addition to producing fewer mature B cells than the wild-type mice, the VpreB-deficient mice generate B cells as shown on the right. What is the explanation of the difference seen between the wild-type and the VpreB-mutant B cells?
- After comparing the whole genome sequencing results from a candidate that you suspect has a mutation that causes a downstream shift in start site selection to the parent strain to rule out pre-existing mutations, you are left with the following list of missense mutations. In 100 words or less, explain which of these mutations you believe is likely responsible for the transcription-related defects observed in your candidate strain and why you have ruled out the others.SWH1 D338V TFA1 C127R PKC1 I866LIn the module, you have learned about P-element mediated transgenesis in Drosophila and the concept of using transgenes to rescue mutant phenotypes. In the figure below, you will see a wild type fly with its natural eye colour and three mutants with their eye colours changed to vermillion, white and rosy, respectively. A schematic of P-element mediated transgenesis (as shown in the lectures) is also included in the figure. Please inspect the schematic carefully and choose which of the following statements is true: I. Injection of the white experimental transgene into the vermillion mutant embryo will not change the vermillion mutant phenotype II. Injection of the white experimental transgene in the rosy mutant embryo will change rosy eye colour to red (wild type) III. Injection of the white experimental transgene in the white mutant embryo will not change the white mutant phenotype IV. Injection of the white experimental transgene in the rosy mutant…Analyzing Cloned Sequences A base change (A to T) is the mutational event that created the mutant sickle cell anemia allele of beta globin. This mutation destroys an MstII restriction site normally present in the beta globin gene. This difference between the normal allele and the mutant allele can be detected with Southern blotting. Using a labeled beta globin gene as a probe, what differences would you expect to see for a Southern blot of the normal beta globin gene and the mutant sickle cell gene?