1/67
Public Exam 1
Name | Mastery | Learn | Test | Matching | Spaced |
---|
No study sessions yet.
Eukaryotic
have DNA enclosed in Nucleus
Prokaryotic (bacteria and archaea)
DNA not enclosed in nucleus
What do Prokaryotes and Eukaryotes have in common
have
DNA
RNA and proteins,
metabotically active and
maintain intracellular homeostasis
According to the fundamental cell theory, where do cells arise from?
pre existing cells and through cell division
Historically, organisms were grouped into taxonomic rankings based on ___________, but are now more accurately grouped based on ________________.
morphology
genetic and molecular evidence
What is the evolutionary history of non-nuclear DNA in mitochondria?
mitochondria have their own DNA because they evolved from free-living prokaryotes that became permanent residents inside eukaryotic cells.
Cystic fibrosis is caused by mutations in the CFTR gene, which prevent the function of the chloride channel (a plasma membrane protein) it encodes. What type of phenotype is being described?
cellular phenotype
You are examining the DNA of cells from two mystery organisms. You are trying to determine which of the organisms are more complex. The DNA in cells from mystery organism #1 has about 15,000 genes and a genome size of 1 billion base pairs. The DNA in cells from mystery organism #2 has 14,000 genes and a genome size of 1.2 billion base pairs. Can you predict with certainty which organism is more complex? Why or why not?
no you need
regulatory networks
epiginetic
cell type/ tissue
The CFTR gene is very well conserved from mice to humans. What conclusions can you make about CFTR based on this information?
so important for survival and homeostasis that natural selection has preserved it across species.
Many scientists have studied the function of CFTR in mice? Is the function of CFTR in mice relevant to human CFTR? Why or why not?
yes, because the gene is conserved and serves the same essential role,
Genetic mutations can quickly lead to antibiotic resistant bacteria. Why can antibiotic resistance develop so quickly in bacteria?
short generation times,
big populations,
frequent mutations, and
horizontal gene transfer
Which processes contribute to genetic variability in sexually reproducing organisms?
independent assortment,
crossing over,
random fertilization,
mutations
Based on what you know about genetic variability in sexually reproducing organisms, why is the phrase, “You’re one in a million!” so inaccurate?
independent assortment, crossing over, and random fertilization creates far more than a million possible outcomes. (1 in trillion)
What are the different ways in which new genes are created.
Gene duplication
Exon shuffling
Retrotransposition
Horizontal gene transfer
Gene duplication
extra copies of a gene are made,
one copy can have a mutation and takes on a new function
while the other keeps the original role.
Exon shuffling
recombination: mixes and matches exons (coding regions of DNA), creating new gene combinations.
Retrotransposition
an mRNA copy of a gene is reverse-transcribed back into DNA and inserted into the genome, forming a new gene.
Horizontal gene transfer
DNA from another organism (often bacteria or viruses) is integrated into the genome, adding brand-new genes.
Proteins encoded by genes within the same gene family are often said to have modularity of structure because _______________________________.
they are built from similar functional domains that can be mixed, matched, and reused in different proteins.
What levels of protein structure would be disrupted if hydrogen bonding was prevented in a protein composed of a single peptide
secondary and tertiary levels of protein structure
TCF1 and TCF2 are in the same gene family. TCF1 is a transcription factor that binds to DNA and helps promote transcription. What can you infer about TCF2?
TCF2 also binds DNA and influences transcription
A gene called GSK3 duplicates but does not diverge. What is the result?
two copies of the same gene with the same function
no new function
Why do mutations in the myostatin gene cause increased muscle mass?
no stop signals for muscle precursor cells (myoblasts)
Necrosis
uncontrolled cell death
cells swell, their membranes rupture, and they spill their contents into the surrounding environment
This often causes inflammation and damage to neighboring cells
Apoptosis
programmed cell death
Cells shrink, their DNA condenses, and they break apart into small apoptotic bodies that can be safely removed by phagocytes
without damaging surrounding tissue.
Why is ECM so critical for the health of an organism? (Hint: what functions does the ECM perform?)
provides structure,
supports and binds tissues,
anchors cells,
allows fluid and nutrient exchange
regulates key cell behaviors
You are examining the ECM of a femur (thighbone). Where did the ECM come from? (Is it made up of bone cells? Or was it secreted by bone cells? Or was it produced by surrounding muscle? Or is there a separate explanation?) Hint: you do not need to know about the femur to answer this question; it relates to all ECM.
secreted by bone cells
What are the differences between peptidoglycan and extrapolymeric substance (EPS)?
Peptidoglycan is a cell wall polymer that protects individual bacterial cells.
EPS is a soft, secreted biofilm matrix that protects and organizes bacterial populations
What is quorum sensing?
cell-to-cell communication
uses chemical signals to sense population density and
coordinate group behaviors
Compare and contrast the four major types of signal transduction based on: The types of ligands involved How far the ligands travel between the ligand-producing cell and the responding cell Whether each is considered to be a type of local or systemic signaling
Endocrine signaling is long-distance and systemic,
paracrine, autocrine, and synaptic (rapid) signaling are all local
When a large, multicellular organism needs an efficient, highly targeted, fast, systemic signaling system, which type of signal transduction is used?
Synaptic signaling
Is endocrine signaling considered less efficient than synaptic signaling? Why or why not?
it’s slower and less targeted
What would happen to developing cardiomyocytes in the sinoatrial node (SAN) of an embryonic heart if you removed the SAN ECM from the sinoatrial node and replaced it with ECM from the left ventricle (LV). (In other words, you added LV ECM to the sinoatrial node.)
The wrong ECM cues would disrupt SAN pacemaker development and push cells toward LV-like muscle behavior instead of proper SAN function
What is the type of systemic signaling that always involves short-range diffusion of the ligand?
Endocrine
You are characterizing cells in a tissue section. You have identified a group of cells that perform the primary functional role associated with the tissue, are terminally differentiated, and are tightly connected with very little ECM. What terms would apply to this cell type?
epithelial cells
A scientist looking at a group of cells in an epithelium under the microscope noted that they likely had a role in moving mucus over the cells, were rectangular-shaped, and had nuclei at different heights, but all shared a common basal lamina. What epithelial cell type is the scientist observing?
ciliated pseudostratified columnar epithelium
What specific epithelium is being described in the previous question?
tracheal epithelium
Also relating to the previous question, what function would these cells lose if their cilia were not functioning?
could no longer move mucus, causing a loss of airway cleaning and defense.
Why do gut and tracheal epithelia have tight junctions?
seal the cells together to stop leaks and block germs from getting through
What are the main connective tissues and their cells?
Adipose → adipocytes;
Cartilage → chondrocytes
Bone → osteoblasts, osteocytes, osteoclasts
Blood → RBCs, WBCs, platelets
Fibrous CT → fibroblasts
Does dense connective tissue have low or high ECM compared to cells?
High ECM
What happens if osteoclasts are too active? Too many osteoblasts?
Extra osteoclasts → bone loss/weak bones.
Extra osteoblasts → overly dense or excess bone growth.
What are osteoclasts?
Osteoclasts break down bone
What are osteoblasts?
osteoblasts build bone
What phenotype would occur if there was a decrease in myelin-producing cells? (i.e., how would loss of myelin affect neuronal function?)
Loss of myelin slows or blocks action potentials, impairing neuron communication
ECM molecules can function as ligands in a type of signaling referred to as _________________________________ signaling. Another type ligands called __________________________________are specifically involved in endocrine signaling; these ligands reach responding cells by travelling through __________________________________. Another type of signaling referred to as ________________________________ signaling involves ligands being secreted and diffusing locally through the ECM. Finally, ____________________________________are the name for ligands that function in synaptic signaling.
ECM molecules can function as ligands in a type of signaling referred to as contact-dependent signaling
Another type ligands called hormones are specifically involved in endocrine signaling; these ligands reach responding cells by travelling through the bloodstream
Another type of signaling referred to as paracrine signaling involves ligands being secreted and diffusing locally through the ECM
Finally, neurotransmitters are the ligands that function in synaptic signaling
Adipose tissue is considered to be __________ connective tissue because it has __________ ECM relative to cells.
Loose connective tissue
less ECM relative to cells.
Cartilage is considered to be __________________________ connective tissue because it has _________________________________ ECM relative to cells. The mature cell type that makes up the cellular matrix on cartilage is called a__________________________________.
Dense connective tissue
abundant ECM relative to cells
chondrocyte.
What is the role of TFII transcription factors? How do they function? What would the consequence be if all TFIIs stopped functioning in a cell?
They recruit RNA polymerase II and start transcription; without them, no mRNA is made and the cell dies.
According to the histone-code hypothesis, what is one way that cell specialization occurs?
Different histone modifications change chromatin structure and gene expression, creating cell-specific patterns that drive specialization .
Lactose intolerant individuals do not produce the enzyme lactase. Studies show that the gene that encodes lactase is not transcribed. Describe the conformation of the nucleosomes (condensed or uncondensed) surrounding this gene and the potential histone modifications that could cause this conformation?
Its nucleosomes are condensed, caused by histone deacetylation and/or repressive histone methylation.
What would happen if a lysine residue that was normally acetylated was mutated to an arginine? How would this change affect the nucleosome and what would the consequence be for gene expression? (Note: arginine is a positively charged amino acid that cannot be acetylated; for the purpose of this question, assume this arginine is not subject to methylation.
he nucleosome stays condensed (positive charge maintained), so the gene is repressed and transcription decreases.
What happens to gene expression if…
Overactive histone acetyltransferases
gene expression increases
What happens to gene expression if…
Overactive histone deacetylase
Gene expression would decrease.
What happens to gene expression if…
Overactive histone methyltransferases
not predictable
What happens to gene expression if…
Impaired histone acetyltransferases
Gene expression would decrease.
What happens to gene expression if…
Impaired histone deacetylases
Gene expression would increase
What happens to gene expression if…
Impaired histone demethylases
not predictable
How do enhancers affect gene expression?
They bind tissue-specific transcription factors, open chromatin, and stabilize the transcription initiation complex to increase gene expression.
What proteins are required for transcription of all genes expressed in all cells, regardless of cell-type?
The TFII general transcription factors and RNA polymerase II.
Is an individual enhancer able to bind more than one transcription factor? What is the advantage of this?
Yes; it allows flexible, precise regulation of when, where, and how strongly a gene is expressed.
What does the stability of the transcription initiation complex determine?
It determines how much RNA Pol II is recruited and therefore how many transcripts are made
NCAM is a gene that is normally only transcribed in neurons. What are the ways that you could induce (force) expression of NCAM in muscle cells?
Add a neuron tissue-specific transcription factor to muscle, or mutate the NCAM enhancer so it binds a muscle tissue-specific transcription factor
TGFb is a gene that is normally expressed in retinal cells. What are the ways that you could inhibit expression of TGFb in retinal cells?
Mutate or block its enhancer so retinal transcription factors can’t bind, add repressive histone modifications, or methylate the DNA to keep chromatin closed
TGFb is expressed in retinal cells, but not cornea cells. How is it that TGFb is normally expressed in retinal cells, but not cornea cells?
Retinal cells have transcription factors that bind the TGFβ enhancer; cornea cells do not
What is an epigenetic reason that Cav1 might not be transcribed?
Cav1 chromatin closed by histone/DNA modifications
What is a genetic reason that Cav1 might not be transcribed?
Mutation in Cav1 promoter/enhancer prevents TF binding.
“All other genes in the osteoblast are appropriately transcribed.” What potential reasons are ruled out by this statement?
General transcription machinery defects (RNA Pol II, TFII factors, global chromatin).