5.Once mTORC1 is activated, it displays protein kinase activity. It phosphorylates the hy-droxy group on serine residues on substrate proteins, many of which are involved in controlling geneexpression, via the reaction:MTORC1 + ATP + substrate(Ser-OH) → MTORC1 + ADP + substrate(Ser-PO4)(a) Describe how serine is synthesized in mammalian cells including precursors, intermediates andenzymes. Where does the amino group come from?(b) Once mTORC1 has phosphorylated a serine residue on its substrate, the substrate has a phos-phoserine side chain. Is this phosphoserine side chain different than the side chain of the serine bio-synthetic intermediate 3-phosphoserine, and, if so, how?(c) When mTORC1 is inhibited by the drug rapamycin, cells perform large-scale catabolism of cyto-solic and organellar proteins by proteases in the lysosome. If a protein is phosphorylated on a serineresidue and undergoes degradation in the lysosome, phosphoserine can be released back to the cy-tosol. What are the possible metabolic fates of this liberated phosphoserine?

Phosphates called the alpha, beta, gamma phosphates. ATP are much lesss firmly attached, and some…

Answered: 5. Once mTORC1 is activated, it…

Human Anatomy & Physiology (11th Edition)

11th Edition

ISBN:9780134580999

Author:Elaine N. Marieb, Katja N. Hoehn

Publisher:Elaine N. Marieb, Katja N. Hoehn

Chapter1: The Human Body: An Orientation

Section: Chapter Questions

Problem 1RQ: The correct sequence of levels forming the structural hierarchy is A. (a) organ, organ system,...

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Now read this abstract from a 2013 journal article What is the authors' explanation of how Gal80p works? Note UASG from the question above is the same as UASGAL The DNA-binding transcriptional activator Gal4 and its regulators Gal80 and Gal3 constitute a galactose-responsive switch for the GAL genes of Saccharomyces cerevisiae. Gal4 binds to GAL gene UASGAL. (upstream activation sequence in GAL gene pro- moter) sites as a dimer via its N-terminal domain and activates transcription via a C-terminal transcription activation domain (AD). In the absence of galactose, a Gal80 dimer binds to a dimer of Gal4, masking the Gal4AD. Galactose triggers Gal3-Gal80 interaction to rapidly initiate Gal4-mediated transcription activation. Just how Gal3 alters Gal80 to relieve Gals0 inhibition of Gal4 has been unknown, but previous analyses of Gal80 mutants suggested a possible competition between Gal3-Gal80 and Gal80 self-association interactions. Here we assayed Gal80-Gal80 interactions and tested for…
Drug X shown below is a kinase inhibitor used to treat multiple types of breast cancer. Breast cancer cells are treated with the drug and after 8 hr are lysed and the presence of various proteins is shown by a band on a western blot. The presence of the phosphorylated form of the protein is shown by the presence of a band when probed with antibodies that recognize the phosphorylated form of protein and are indicated by a p- in front of protein name (e.g. p-AKT). Based on this information, which kinase is likely the target and is inhibited by Justify your answer in 3-4 sentences. Drug X. F FF N. -N S IZ H₂N `N No Drug (+) Drug p-AKT AKT p-GSK3B GSK3B p-p70S6K p70S6K
Which of the following statements is true regarding the two primary classes of chaperone protein complexes in eukaryotes? O both require ATP to function, but hsp70 interacts with protein targets while they are being translated O neither require ATP, but both interact with protein targets simultaneously O hsp60 complexes are huge, and interact with protein targets during translation Ohsp70 interacts with fully synthesized proteins
The diagram below shows a closeup of regulatory proteins binding to one of the UASG elements near the GAL7, GALI0, and GALI genes, which code for the protein products needed for yeast to use the sugar galactose. The red triangle symbolizes an "effector" molecule that binds to Gal80p. In this hypothesis (which has since been shown to be incorrect), what could be happening to Gal80p when it is bound to the effector molecule that causes it to change its position and uncover the Gal4p transcriptional activation domain. Hint: think about what effector molecules do upon binding to proteins such as the the Lac repressor protein or the CAP protein. Galactose absent, glucose absent Gal80p. _Activation domain Gal4p dimer -Binding domain UASG Galactose present, glucose absent Activation domain Gal80p- Binding domain UASG For the toolbar, press ALT+F10 (PC) or ALT+FN+F10 (Mac).
Searching the yeast Saccharomyces cerevisiae genome, researchers found approximately 4,000 DNA sites with a sequence which could potentially bind the yeast transcription factor GAL4. GAL4 activates the transcription of galactose genes. Yet there are only 10 GAL4-binding sites which control the genes necessary for galactose metabolism. The GAL4 binding sequence is CGGAT#AGAAGC*GCCG, where # is T, C or G, and * is C or T. In one chromatin immunoprecipitation experiment (ChIP), yeast growing on galactose were lysed, and subjected to cross-linking reagents which cross-linked transcription factors and activators to DNA. Next the DNA was sheared into small fragments, and antibodies to GAL4 were added. These antibodies coprecipitated the GAL4 and the DNA it was cross-linked to. The cross-linking was then chemically reversed, and the DNA was isolated, cloned into a library of plasmids and sequenced. Results showed that only 10 different DNA sequences had GAL4 bound. Since the…
1. Which of the following signaling events is NOT engaged downstream of phospholipase C (PLC)-gamma activation? a. Calcium ion (Ca2+) release from the endoplasmic reticulum (ER) b. Heterodimerization of the subunits c-Fos and c-Jun to form the transcription factor AP-1 c. IkappaB degradation and resulting translocation of NFkappaB into the nucleus d. Recruitment of protein kinase C (PKC)-theta to the plasma membrane e. PIP3 generation at the plasma membrane which recruits and activates Akt, leading to cytoskeletal remodeling
You are researching the regulation of cell-size control and discover that a signaling pathway that acts through a particular enzyme-coupled receptor is important for the size growth (enlargement) of rat kidney cells. Receptor activation causes activation of adenylyl cyclase, which ultimately leads to the activation of PKA. PKA then phosphorylates a transcription factor called BTS on threonine 84. This phosphorylation is required to allow BTS to bind to specific regulatory DNA sequences, increasing the transcription of Zrt2, a gene encoding a protein vital for kidney cell growth. You find that kidney cells without this receptor are 25% smaller than normal cells. When you measure cells expressing a constitutively active version of PKA, you find they are 25% bigger than normal kidney cells. Based on these results, predict whether a kidney cell’s size would be bigger or smaller than normal kidney cells in each of the following circumstances. Explain why in 1-2 sentences for each. You add…
You are researching the regulation of cell-size control and discover that a signaling pathway that acts through a particular enzyme-coupled receptor is important for the size growth (enlargement) of rat kidney cells. Receptor activation causes activation of adenylyl cyclase, which ultimately leads to the activation of PKA. PKA then phosphorylates a transcription factor called BTS on threonine 84. This phosphorylation is required to allow BTS to bind to specific regulatory DNA sequences, increasing the transcription of Zrt2, a gene encoding a protein vital for kidney cell growth. You find that kidney cells without this receptor are 25% smaller than normal cells. When you measure cells expressing a constitutively active version of PKA, you find they are 25% bigger than normal kidney cells. Based on these results, predict whether a kidney cell’s size would be bigger or smaller than normal kidney cells in each of the following circumstances. Explain why in 1-2 sentences for each. You…
A -------| B-------> Violet A linear switch-regulation pathway of the type shown here controls flower color in a certain species. The wildtype color is violet, but mutants can be either white or purple. Gene products A and B act in the pathway at the positions and in the manner shown (A is inhibitory, B is intensifying). A and B are the products of genes A and B, respectively. What are the expected phenotypes of: (a) A loss-of-function mutation in A? (b) A gain-of-function mutation in A? (c) A loss-of-function mutation in B? (d) A gain-of-function mutation in B?
RGS proteins accelerate the GAP activity of Gα subunits. What is the direct result of this GAP activity? - hydrolysis of GTP, resulting in a GDP-bound Gα - phosphorylation of GDP to GTP, resulting in a GTP-bound Gα - an exchange of GTP for GDP bound to Gα - an exchange of GDP for GTP bound to Gα
3). Consider the four mutations (i-iv) described below: i. One of the mutations causing cystic fibrosis in humans is a deletion of three nucleotides that eliminates a phenylalanine at position 508 of the CFTR protein (D508). Normally, CFTR protein is localized to the plasma membrane, where it functions as a chloride ion channel. D508 CFTR is misfolded and all of it is degraded without ever reaching the cell surface. ii. The yeast transcription factor Gal4p contains a DNA-binding domain and a transcriptional activation domain. An allele with a deletion the gene portion encoding the activation domain encodes a truncated Gal4p containing only the DNA-binding domain. It binds to Gal4p target genes at appropriate binding sites in their upstream regulatory regions, but does not activate their transcription. In cells with both wild type and mutant forms of Gal4p, the truncated Gal4p binds more efficiently to target DNA sequences than wild type. iii. Mutations in the acid maltase gene in…
1. Peroxisomes are organelles surrounded by a single membrane. Soluble proteins that reside within peroxisomes are imported post-translationally, and they often contain the C-terminal tripeptide SKL (serine-lysine-leucine). a. How would you confirm that a C-terminal SKL tripeptide is a peroxisomal targeting signal? b. If cells were engineered to produce a hybrid protein consisting of a mitochondrial matrix protein (including its signal sequence) followed by a C-terminal SKL signal, where in the cell would you expect the hybrid protein to be found? Explain your reasoning. 2. Functional mitochondria can be isolated from cells. These isolated mitochondria are used to study oxidative phosphorylation and the import of proteins into the matrix. In an appropriate buffer, isolated mitochondria will rupture to generate “mitoplasts” in which the inner membrane remains intact but the outer membrane is lost. Would you expect mitoplasts to support oxidative phosphorylation?…

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