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Biol 300 > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

What is extracellular matrix?

A

-structure: 3D framework of fibers of proteins and glycoproteins
-function: maintains a useful 3D arrangement of tissues in body

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2
Q

What is ground substance?

A

aqueous gel of glycoproteins and proteoglycans that occupies the space between cellular and fibrillar elements of connective tissue.

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3
Q

What are proteoglycans?

A

a core protein and its covalently attached GAGs

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4
Q

What is a GAG?

A

a linear sequence of monosaccharides that is covalently attached to core protein

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5
Q

What is Hyaluronate?

A

polysaccharide to which proteins bind non-covalently

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6
Q

What are 3 different GAG names?

A

Keratan sulfate, chondroitin sulfate, and hyaluronate

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7
Q

What is the source of molecules of the ECM and ground substance?

A

cells

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8
Q

What is the level of organization in a human?

A

cells -> tissue -> organ -> organ system -> organism

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9
Q

What are tissues?

A

different types of cells comprise a tissue

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10
Q

What is an organ?

A

different types of tissues comprise an organ

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11
Q

What is an organ system?

A

different types of organs comprise an organ system

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12
Q

What is an organism?

A

different types of organ systems comprise an organism

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13
Q

What are the 4 types of tissues?

A

-nervous tissue
-epithelial tissue
-muscle tissue
-connective tissue

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14
Q

What is the general structure of connective tissue?

A

-ECM
-ground substance
-cells that hold onto the framework that include fibroblasts

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15
Q

What are some functions of fibroblasts?

A

-secretion of molecules for ECM
-secretion of cytokines

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16
Q

What are cytokines?

A

signaling molecules that coordinate the activity of immune cells, to include movement, differentiation, and division

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17
Q

What type of tissue is blood?

A

connective tissue

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18
Q

What is hematocrit?

A

percentage of blood that is occupied by erythrocytes (RBCs)

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19
Q

What is differentiation?

A

a change in the gene transcription pattern of a cell that ultimately resulting changes in appearance, capacities, behavior, etc..
-with very rare exceptions, every human cell have every human gene, they’re just not always expressed.

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20
Q

How do genes contribute to erythropoiesus?

A

-erythrocytes from stem cells
-stem cell divides -> 1 daughter cell (stem cell) 1daughter cell (differentiated)
-HSCP -> HSC -> CPC -> MPC -> erythrocytes

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21
Q

What is biological source of erythrocytes?

A

-lots of cell division, but daughter cells keep differentiating until erythrocytes -> then no more division just differentiation
-terminally differentiated cell at orthochromatic erythroblastc

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22
Q

Can we breathe easily everywhere?

A

no!

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23
Q

What is hypoxia?

A

-condition in which cells do not receive sufficient oxygen to function normally, or to survive

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24
Q

What is the minimum partial pressure of oxygen for normal human function?

A

14.5kP (109 mmHg) around 2,500m

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25
Q

What are 4 major cells, tissues, and organs that contribute to our response to hypoxia?

A

-lungs
-erythrocytes
-kidneys
-bones

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26
Q

What role do lungs play in body’s response to hypoxia?

A

oxygen diffuses from atmosphere to bloodstream

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27
Q

What role do erythrocytes play in body’s response to hypoxia?

A

majority of oxygen cargo is carried by intracellular hemoglobin

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28
Q

What role do kidneys play in body’s response to hypoxia?

A

fibroblasts detect oxygen concentration

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29
Q

What role do bones play in body’s response to hypoxia?

A

erythrocytes proliferate, generating more erythrocytes

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30
Q

Where does process of erythrocyte production start and end?

A

-the process begins in the kidney fibroblasts
-the process ends in the bone marrow erythroblasts

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31
Q

How do our bodies generate erythrocytes?

A

-kidney synthesize and secrete erythropoietin (EPO)
- EPO gets dumped into bloodstream
-then blood goes to stem cells in bone marrow

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32
Q

What should you know about the structure of the kidney?

A

-outer layers of kidney = cortex
-nephron = filters stuff out of blood

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33
Q

Is oxygen uniform throughout the kidney?

A

no

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34
Q

What are agents of oxygen detection?

A

kidney fibroblasts
-fibroblasts in normoxic conditions are around medulla
-fibroblasts move to higher oxygen concentration and make more EPO at hypoxia

35
Q

What molecule in a kidney fibroblast is the oxygen sensor?

A

PHD2
-needs Fe +
–H313
–D315
–H374
-when folded, they’re close together and become oxygen sensor

36
Q

What is hypoxia-inducible factor 1 alpha? (HIF-1alpha)

A

a transcription factor
-red segment: necessary for binding to DNA
-blue segment: necessary for binding to HIF-1 beta
-3 targets for covalent modification:
–Pro 402
–Pro 563
–Asn 804

37
Q

How do PHD2 and HIF-1a interact?

A

PHD2 carry Fe ion and ascorbate (vit C) -> interacts w/ HIF-1a carrying O2 -> PHD2 hyroxylates HIF-1a -> HIF-1a now haws Pro that is hydroxylated
– in presence of sufficient concentration (normoxic conditions) of O2, this is always happening in kidney fibroblasts

38
Q

What is HIF-1beta?

A

forms a heterodimer with HIF-1a to create HIF-1
-bond noncovalently
-red segment: necessary for binding to DNA
-blue segment: necessary for binding to HIF-1a

39
Q

What happens when a protein is ubiquinated?

A

a ubiquinated protein is targeted for recycling by proteosomes
-3 enzymes: E1, E2, E3

40
Q

What is ubiquitin?

A

a small protein that can be covalently attached by an enzyme to a target protein

41
Q

What is a proteasome?

A

multiprotein complex that digests proteins into amino acids and oligopeptides
-tube made of multiple proteins
-proteins that enter tube are about to be recycled
-goes in protein -> comes out amino acid

42
Q

How is HIF-1a activity regulated?
(normoxic conditions)

A

in normoxic conditions, oxygen is present and PHD2 can use Fe to just grab O2 and hydroxylate Pros -> have hydroxyl group now so can bind to VHL -> can recruit E1, E2, & E3 -> HIF-1a destroyed

43
Q

How is HIF-1a activity regulated?
(hypoxic conditions)

A

in hypoxic conditions, there’s not enough oxygen around -> if PDH2 doesn’t get enough oxygen -> not all HIF-1a gets hydroxylated -> concentration of HIF-1a increases -> HIF-1a binds to HIF-1B -> form HIF-1 and acts as TF -> bind to specific seq of DNA that bind to promoters of certain genes -> upregulate/downregulate certain genes

44
Q

What does binding to VHL lead to?

A

when concentration of O2 is low -> genes of EPO are transcribed and translated -> which is involved in stimulating erythroblasts to make more erythrocytes (RBCs)

45
Q

What does HIF-1a do when active?

A

in hypoxic conditions -> create HIF-1 and bind to HRE -> other end can bind to P300

46
Q

What is P300?

A

Histone Acetyl transferase (HAT)
-transcriptional co-activator
-acetylates histones ->brings no charge so DNA is more accessible

47
Q

What is the core nucleotide sequence of HRE?

A

5’-RCGTG-3’

48
Q

What is EPO?

A

structure: glycoprotein
function: cytokine
-detect decrease of oxygen

49
Q

What is EPOR?

A

homodimer
~erythrocytes in bone marrow receive signal~
-EPOR needs to bind noncovalently to JAK 2 so receptor will be phosphorylated at tyrosine

50
Q

What is structure of JAK 2?

A

kinase (take P from ATP and phosphorylates)
-FERN binds noncovalently to EPOR

51
Q

What is the structure of STAT5?

A

there are 7 different types of STAT proteins
-dimers of STAT proteins are TFs

52
Q

How does EPOR respond to EPO binding?

A

FERN is bound to EPOR receptor -> signal comes from EPO -> EPO changes shape (shifted) and kinase is activated

53
Q

What happens after EPO binding at EPOR?

A

EPO binds -> causes 2 receptors to bind to each other -> JAK 2 activates and phosphorylates other JAK 2 -> og JAK 2 gets phosphorylated -> JAK 2 will phosphorylate tyrosine in own receptor -> now docking sites for STAT 5 -> STAT 5 binds and gets phosphorylated by JAK 2 -> STAT 5 lets go -> new STAT 5 comes along -> repeats until SHP1 comes along and binds to phosphorylated JAK 2 and starts dephosphorylating receptor

54
Q

What is one target gene of STAT 5?

A

BCL-XL
anti apoptotic protein

55
Q

What is apoptosis?

A

cell suicide = orderly form of self destruction
cell shrinks -> molecules digest themselves -> membrane doesn’t break -> form blebs -> break off into little vesicles and hands to neighbors for them to phagocytize blebs

56
Q

How is apoptosis regulated?

A

collection of proteins, either pro or anti apoptosis and depending on signals received, cell would respond either way

57
Q

What should you know about BCL-XL?

A

BCL-XL is anti apoptotic so it is pro life
-2 pro apoptosis proteins: BAK and BAX

58
Q

How does BCL-XL interact with BAX?

A

BAX and BCL-XL bump into each other and bind -> leave membrane and go to cytoplasm -> leave and break apart
-this cycle only continues if equal numbers of BAK and BCL-XL
-if not enough BCL-XL then BAX keeps building on itself and build pore in membrane

59
Q

If BCL-XL is insufficient to keep BAX in cytoplasm, and if pro-apoptotic signals arrive, then what does BAX do?

A

pore or opening extends through both membranes -> goes through mitochondrial membrane
~ kinda like attacking energy plants in war ~

60
Q

What happens when BAX and/or BAK are allowed to dimerize?

A

Cyt C is gonna leave intermembrane space

61
Q

Why is Cyt C important?

A

it is key participant in life-supporting function of ATP synthesis
-cyt c is released from mitochondria -> binds to apaf-1 -> oligomerization -> forms pro-caspase 9 -> apoptosome -> interacts with pro-caspase 3 -> apoptosis

62
Q

How is hypoxia tie in with BCL-XL?

A

hypoxia results in an increase of expression of BCL-XL in erythroblasts

63
Q

How is cell cycle regulated?

A

cyclins
-CDKs (cyclin dependent kinases)

64
Q

What is cyclin E?

A

2 important functions:
-interacts with CDK2 protein kinase to form serine/threonine-kinase holoenzyme complex
-the cyclin subunit imparts substrate specificity to the complex

65
Q

What is CDK2?

A

1 function:
serine-threonine protein kinase

66
Q

How do cyclin E and CDK2 interact?

A

they comprise a holoenzyme

67
Q

What are the results of the cyclin E and CDK2 holoenzyme?

A

-can inhibit cell cycle inhibitors
-activating cell-cycle activators
-RB1: retinoblastoma-associated protein

68
Q

What are E2F proteins?

A

transcription factors

69
Q

Where does DNA replication begin?

A

ori site: specific seq of nucleotides

70
Q

Are there ori sequences in EUK?

A

yes for some, no for others

71
Q

What do researchers think contribute to functional replication origins?

A

-TFs
-sequence motifs in DNA
-histone modifications

72
Q

What happens at an ori site?

A

2 strands at ori site are separated
by other agents
-RNA primer (5-10nt) allows new strands to be built off of template
~lagging strands can be 1,000-2,000nt in prokaryotes and 100-200nt in euk~

73
Q

What are the 2 steps that initiate DNA replication?

A

-origin licensing
-origin firing

74
Q

What happens at origin licensing?

A

ORC -> CDC6 -> Cdt1

75
Q

What happens at origin firing?

A

MCM2-7 double hexamer
one ->DDK ->CDK
the other: CDC45 -> GINS etc..

76
Q

What is the ORC?

A

multi-protein complex made out of 6 proteins arranged roughly symmetrically, arranged in a ring to circle the ori
-ORC 1, ORC 2, ORC 3, ORC 4, ORC 5, CDC 6

77
Q

Can ORC proteins interact with chromatin?

A

yep!
-bind and create a chain of binding from nucleosome histones to ORC proteins

78
Q

What is the MCM complex?

A

the catalytic core of a larger helicase complex that unwinds parental DNA
-made of ring shaped structure with 6 proteins: MCM2-MCM7

79
Q

How is a pre-replicative complex (pre-RC) assembled?

A

ORC1-5
ORC 6
CDC 6
CDT1
MCM2-7
ORC1-6 and CDC6 bind -> then bind to DNA -> CDT1 causes MCM2-7 to open and slip around double stranded DNA -> then closes up again

80
Q

When is a pre-RC assembled?

A

in the G1 phase
-assembly of a pre-RC requires cyclin E

81
Q

What is the GINS complex?

A

-structure: a complex of four proteins -function: that mediates the assembly of replication factors around the MCM helicase during DNA replication

82
Q

What is a CMG helicase complex?

A

-structure: CDC45, MCM2-7, and GINS
-function: separation of DNA strands

83
Q

How are CMG complexes assembled?

A
84
Q

How is the dsDNA duplex melted?

A

both MCM complexes contribute to the separation of DNA strands

Biol 300 (6 decks)

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