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Final Exam deck Flashcards

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Biology 101 flashcards
1
Q

Cell membrane lipid composition is largely composed of these three components.

A

Phospholipids, Glycolipids, and Cholesterol

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2
Q

What does cholesterol do to membrane fluidity?

A

“Alters” it, more specifically it stabilizes it. At low temperatures it increases the fluidity, at high temperatures it decreases it.

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3
Q

What do unsaturated fatty acids do to membrane fluidity?

A

Due to their kinks, membrane fluidity is increased because the fatty acid tails are not able to interact as closely. (Saturated fatty acids do the opposite and decrease membrane fluidity)

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4
Q

There are two leaflets of the plasma membrane, what is an example of a unique component on the cytosol side?

A

Phosphatidylserine- note that if this component is present on the side of the extracellular space, it signals that the cell has died and needs to be phagocytized.

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5
Q

There are two leaflets of the plasma membrane, what is an example of a unique component on the extracellular side?

A

Glycolipids

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6
Q

How is asymmetry of the two leaflets of the plasma membrane maintained?

A

Actively

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7
Q

Membranes can be laterally non-uniform, presence of a tight junction enables what?

A

Apical-basolateral cell polarization (Different proteins on the apical surface vs basal and lateral surfaces)

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8
Q

How are ions (small charged molecules) moved across the cell membrane?

A

Transporters and channels

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9
Q

Which molecules move across the cell membrane without requiring facilitated transport?

A

Hydrophobic molecules ie O2, CO2, N2, benzene (move easily) and small uncharged polar molecules ie water, urea, glycerol (move slightly less easily)

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10
Q

What type of ion channel is always open? Which ion is known for having leak channels in the cell membrane?

A

Leak channels, Potassium ions

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11
Q

What type of ion channel is not always open? What are the two types of this ion channel and what signals them to open and what ions can pass through these channels?

A

Gated ion channels.
Voltage gated- signaled by a change in membrane potential, potassium and sodium ions
Ligand gated- signaled by a ligand (molecule that binds to another molecule) binding to the channel, sodium ions.

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12
Q

What is the electrochemical gradient and what are the definitions of each of its components?

A

The summation of both the electrical gradient (electrical difference between inside and outside of the cell= membrane potential) and the chemical gradient (difference in concentration of an ion inside and outside of the cell)

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13
Q

Which side of the cell membrane is more negative? Why?

A

The inside/cytosolic side, negatively charged ions like chloride are trapped inside the cell.

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14
Q

What determines how permeable a membrane is to ions?

A

Whether there are OPEN channels present for said ions.

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15
Q

At rest where are sodium and potassium levels high?

A

Sodium: highly concentrated outside the cell (due to the diligent work of the sodium potassium ATPase pump)
Potassium: highly concentrated inside the cell (due to the negative charge inside the cell- does not continue to flow in because of the chemical gradient)

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16
Q

What is hyperkalemia and what effect does it have on the resting membrane potential, action potentials, and the electrochemical gradient?

A

Increased extracellular potassium levels.
Increasing potassium outside the cell shifts the chemical gradient resulting in more potassium entering the cell.
This makes RMP more positive
This results in it being easier to generate an action potential (but also more difficult to repolarize/reset sodium channels)

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17
Q

What is hyponatremia and what effect does it have on the resting membrane potential, action potentials, and the electrochemical gradient?

A

Decreased extracellular sodium levels.
Decreasing sodium on the outside of the cell results in less driving force for sodium to move inside the cell.
This does nothing to the RMP because potassium leak channels allow potassium to compensate by increasing in concentration inside the cell.
This results in no change for amount of stimulus required to reach threshold but a decrease in the size of the action potential.

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18
Q

What is the cause of acute water intoxication? What happens on the cellular level?

A

Hyponatremia. Extracellular sodium being decreased results in water flowing into the cells (osmotic pressure), resulting in them rupturing.

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19
Q

What is glycocalyx made of?

A 
Glycoproteins (polysaccharides attached to proteins)
and
Glycolipids (polysaccharides attached to lipids)
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20
Q

Which side of membrane proteins are carbohydrates attached to and why?

A

The extracellular side. This is because the carbohydrates are attached inside the lumen of the ER and Golgi. When vesicles are created and transported to the cell membrane, their insides open up to the outside of the cell.

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21
Q

Glycoproteins are structurally complex, their diversity is derived from the following:

A

The amino acid sequence of the protein can vary
The amount of the protein embedded in the membrane can vary
The height and thickness of the saccharide portion can vary

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22
Q

What are three functions of the glycocalyx? (Dr Beck mentioned these)

A

Immune recognition, protective barrier, pathogen receptor

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23
Q

How does the glycocalyx differ between the absorptive and antigen sampling (M) cells of the intestinal epithelium? Which is more susceptible to bacterial infection?

A

The glycocalyx is thicker on the absorptive cells, M cells are more susceptible to bacterial infection.

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24
Q

How does the glycocalyx affect the flu virus’ transmission?

A

Certain glycoproteins are attachment sites for flu viruses. Location of these glycoproteins can affect transmission. (Highly concentrated in upper respiratory=more contagious vs highly concentrated in lower respiratory= less contagious- but in the case of H5N1, also very fatal)

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25
Q

Is ECM (extracellular matrix) a component of cells? What type of tissue has a lot of ECM?

A

No, ECM is secreted by cells but is not actually part of them. Connective tissue.

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26
Q

What are the three components of ECM?

A
  1. Glycose Amino Glycans (GAGs)
  2. Fibers (mostly collagen)
  3. Non-collagen glycoproteins
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27
Q

How much space do GAGs occupy?

A

Most of the ECM! Even though they are less than 10% of the ECM by weight.

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28
Q

Are GAGs positively charged, negatively charged, or neutral and what effect does this have on the ECM?

A

Negatively charged. This charge tends to pull ions like sodium into the ECM, resulting in water also flowing into the ECM, making for a good cushion that provides resistance to compression.

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29
Q

When a GAG is attached to a protein, what is it called. Is this common?

A

A proteoglycan. Yes, most GAGs are attached to proteins.

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30
Q

Is hyaluronic acid a proteoglycan? Where is it present?

A

No, it is a GAG without a protein attached. HA is present in the skin to keep it plump and in joints to keep them well lubricated.

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31
Q

Why is Shar Pei skin the way it is?

A

Overproduction of HA results in very plump (and slimy on the inside) skin.

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32
Q

What kind of strength do collagen fibers provide to the ECM?

A

Tensile

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33
Q

Why do people with Ehlers Danlos Syndrome have stretchy skin?

A

They lack the protease which converts pro-collagen to collagen (ADAMTS2).

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34
Q

What are the elastic fibers of the ECM made up of?

A

Microfibrils (made of a scaffold of fibrillin) supporting elastin molecules structurally.

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35
Q

Where are elastic fibers abundant?

A

Aorta, ligaments, zonular fibers of the eye

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36
Q

Which disease examples did Dr Beck provide regarding issues with elastic fibers?

A

Primary Lens Luxation

Marfan syndrome (mutation in fibrillin), at high risk of aortic aneurism

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37
Q

How long does it take to alter transcription via intracellular signaling?

A

Hours to days

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38
Q

How long does it take to alter protein function via intracellular signaling?

A

Seconds to minutes

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39
Q

How long does it take to alter membrane permeability via intracellular signaling?

A

Milliseconds to seconds

40
Q

What are the two molecular switches which control protein activity?

A

Phosphorylation and GTP binding.

41
Q

At an active chemical synapse, what kind of cell surface receptor is the acetylcholine receptor?

A

A transmitter-gated ion channel. It opens when the signal molecule binds to the receptor.

42
Q

What do G Protein Coupled Receptors (GPCRs) activate and what are the subunits of the thing they activate?

A

Trimeric G Proteins
There is an alpha, beta, and gamma subunit. When activated, the alpha subunit separates from the other two.
The activated trimeric g protein can then activate downstream things.

43
Q

What kind of receptor is the (H1) Histamine receptor?

A

A GPCR (G protein coupled receptor), the alpha subunit of the trimeric g protein cleaves PIP2, producing IP3 and DAG which activate protein kinase C, resulting in itching and swelling

44
Q

What kind of receptors are receptor tyrosine kinases (RTKs) and how are they activated?

A

RTKs are enzyme linked receptors, they are activated via dimerization which occurs when a single signal molecule binds to the extracellular domain.

45
Q

In the inactive state, what is bound to Ras and other GTP binding proteins?

A

GDP

46
Q

What do guanine nucleotide exchange factors (GEFs) do?

A

Remove GDP from GTP binding proteins (like Ras) so that GTP can bind and activate the protein.

47
Q

What do GTPase activating proteins (GAPs) do?

A

Convert GTP to GDP, inactivating the protein.

48
Q

How is Ras activated?

A

Via a GEF, recruited by an activated RTK (enzyme linked receptor activated by dimerization)

49
Q

What activates the MAP kinase cascade?

A

Ras

50
Q

What do Pattern Recognition Receptors (PRRs) do?

A
  • Signal innate immune response
  • Recognize Pathogen Associated Molecular Patterns (PAMPs) ie double stranded RNA (viruses) and lipopolysaccharide (bacteria)
51
Q

What do TLRs (toll like receptors, a type of PRRs) activate?

A

NF-kappa-B, which alters the transcription of many genes via interaction in the nucleus

52
Q

What is a direct way to alter gene transcription in the nucleus?

A

Cytokine binds a cytokine receptor which activates JAK kinases, which recruit STAT proteins which dimerize and alter gene transcription in the nucleus

53
Q

What is the difference between endocrine and paracrine cell signaling?

A

Endocrine uses the bloodstream for distribution of the hormone signal while paracrine is a local hormone signal

54
Q

What is the fancy name for growth hormone, where is it produced, and what does it do?

A

Somatotropin, produced in the anterior pituitary. It promotes cell survival, cell growth, and cell proliferation.

55
Q

In humans, why would we supplement growth hormone?

A
  • In children who have a deficiency, to promote “normal” growth and prevent stunting.
  • In bodybuilders, to promote excessive muscle growth
  • In the elderly, to attempt to maintain muscle mass
56
Q

Where is IGF-1 synthesized and when is it produced?

A

In the liver, all throughout life but with declining levels over time.

57
Q

As growth hormone signaling decreases, lifespan _________

A

Increases

58
Q

What is BST and what effect does rBST have when given subcutaneously to dairy cows?

A

Bovine SomatoTropin, it increases the production of IGF-1 in the liver which in turn increases the survival of mammary alveoli, resulting in 11-16% increased milk production.

59
Q

What is the signaling molecule for glycogen breakdown in the muscle? Liver?

A

In the muscle, epinephrine/adrenaline

In the liver, glucagon

60
Q

What converts ATP to cAMP?

A

Adenylyl cyclase

61
Q

During glycogen breakdown, what does cAMP activate? What is the end product of glycogen breakdown?

A

Protein Kinase A, Glucose-1-Phosphate

62
Q

How many subunits does Protein Kinase A have?

A

Four, “a dimer of dimers”

63
Q

How does cAMP affect CREB transcription?

A

cAMP activates Protein Kinase A, which activates CREB via phosphorylation, CREB binding protein then binds the activated CREB and is a transcriptional co-activator.

64
Q

Cholera. What happens when you get it?

A

The alpha subunit of the trimeric G protein gets permanently turned on via a covalent modification by the cholera toxin. This results in adenylyl cyclase doing lots of conversion of ATP to cAMP. The high levels of cAMP open chloride channels, resulting in an efflux of ions and water into the small intestine. This equals lots of diarrhea and dehydration.

65
Q

Where is adrenaline/epinephrine produced and what does it do?

A

In the adrenal medulla, this is the fight or flight hormone so it increases the sort of processes needed to fight or flight (like heart rate, respiratory rate, glucose release from liver, airway expansion) and decreases processes that are not needed (constricts blood vessels to periphery and GI, constricts GI sphincters)

66
Q

What converts cAMP to AMP?

A

Phosphodiesterase

67
Q

Does caffeine inhibit or activate phosphodiesterase? What is the result on cAMP levels?

A

Inhibits, results in greater cAMP levels (and thus also elevated heart rate via cAMP increasing PKA levels)

68
Q

What happens during M phase of the cell cycle?

A

Mitosis things happen
Prophase- condensing of chromosomes
Prometaphase- nuclear envelope breaks down
Metaphase- chromosomes align on the center of the cell
Anaphase- sister chromatids begin to be pulled to opposite sides of the cell
Telophase- the sister chromatids arrive at spindle poles and decondense
Cytokinesis- cytoplasm is divided and one cell officially becomes two

69
Q

What happens during interphase of the cell cycle?

A

G1- growth occurs here
S- where DNA replication occurs
G2- growth occurs here

70
Q

What is the function of cycline dependent kinases (CDKs)?

A

Cyclines (a type of proteins) bind to them to activate them. This only “partially” activates them though. When active, they signal the cell to do things in the cell cycle like beginning the cell cycle, replicating DNA, or beginning mitosis.

71
Q

What does Kinase CAK do?

A

Phosphorylates a CDK-cyclin complex to fully activate it

72
Q

What does Wee 1 Kinase do?

A

Phosphorylates a CDK-cyclin complex to inactivate it (even if CAK kinase has phosphorylated the activation site)

73
Q

What does Phosphatase CDC 25 do?

A

Dephosphorylates the inactivation site that Wee1 kinase phosphorylates, resulting in an activated CDK-cyclin complex.

74
Q

What do CDK inhibitor proteins (CKIs) do?

A

Bind to the active CDK-cyclin complex to inactivate it, examples include p21 and p27

75
Q

How does a CDK-cyclin complex become de inactivated after a CKI acts on it?

A

The protein (CKI) must be degraded, in the case of p27, this is done by E3 ligase SCF

76
Q

What are the cell cycle checkpoints and what happens during them?

A

G1/S- check that environment is favorable for replication
G2/M- Checks that DNA was replicated correctly, and also environmental favorability
M/G1- Checks to make sure all chromosomes are properly attached to the spindle

77
Q

What does retinoblastoma do? At which checkpoint does it act?

A

Causes cell cycle arrest at G1/S checkpoint, is a tumor suppresor

78
Q

What does Ras do? At which checkpoint does it act?

A

Stimulates cell division, acts at G1/S checkpoint.

79
Q

What does p53 do? At which checkpoint does it act?

A

Prevents cell division, acts at G2/M checkpoint

80
Q

What holds sister chromatids together up until anaphase begins?

A

Cohesin

81
Q

What is required to cleave the connection between two sister chromatids during anaphase?

A

Separase

82
Q

Define apoptosis

A

Programmed cell death

83
Q

Apoptosis is required for:

A

Normal developmental processes
Maintaining homeostasis (same number of cells being created must die or a tumor will occur)
As a protective measure (infection with virus, DNA damage, etc)

84
Q

What physically happens to cells during apoptosis?

A

The cells (specifically chosen, usually one or a small cluster) shrink, the cell membrane stays intact, the cytoplasm goes into apoptotic bodies, and inflammation does not occur

85
Q

What physically happens to cells during necrosis?

A

Lots of cells swell, the cell membranes are disrupted, cytoplasm is released into the interstitial space, and inflammation does occur

86
Q

What are apoptotic bodies?

A

Vesicles which take up parts of cells undergoing apoptosis.

87
Q

What must be activated in order for apoptosis to commence?

A

Caspase- cysteine specific aspartate protease that binds at cystein and cleaves at aspartic acid
Caspases break down more than 1000 proteins!

88
Q

What are the two pathways by which Caspases are initiated?

A

Intrinsic pathway- mitochondrial pathway, cell death initiated by leakage of cytochrome C out of the mitochondria
Extrinsic pathway- death receptor pathway initiated by receptors on the outside of the cell

89
Q

What allows cytochrome C to leak out of the mitochondria?

A

Bax

90
Q

How does cytochrome C initiate apoptosis?

A

It binds adaptor proteins to make apoptosomes which recruit caspase.

91
Q

What binds Bax to prevent apoptosis?

A

Bcl2

92
Q

What binds Bcl2 to encourage apoptosis?

A

Bad

93
Q

What is microphthalmia?

A

“small eye”, a proliferation defect where too little proliferation has occurred, is tied to a maternal Vitamin A deficiency

94
Q

What happens if myostatin is mutated?

A

Myogenesis is not inhibited properly and “double muscling” occurs

95
Q

What is it called when apoptosis between digits is incomplete?

A

Syndactyly

Cell Bio (1 decks)

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