Biochemistry/Biology Flashcards
1
Q
AAs
A
memorize structures and names
2
Q
Henderson-Hasselbalch Equation
A
pH=pKa+log[A-][HA]
Association Constant: [A-][HA]
calculate the ionization of a weak acid or amino acid side chain at a particular pH given the pKa.
3
Q
amino group pKa
A
9, becomes neutral above 9
4
Q
carboxylate group pka
A
2, becomes -1 above 2
5
Q
Isoelectric point
A
PH when there is zero net charge
6
Q
bicarbonate (HCO3-) buffer
A
CO2+H20 –> (CA enzyme) H2CO3 –> H+ + HCO3-
7
Q
Phosphate buffer
A
3 ionizible groups, biologically relevant, pKa of 7.2
phosphate in concert with calcium forms hydroxyapatite (bone)
8
Q
most drug pHs
A
weak acid or weak bases
need to be able to transport across membranes
9
Q
AA structures 1,2,3,4
A
1: AA sequence
2: alpha helical, Bturn/sheet, mixed a/b, random coil
alpha sheet (H bond between, peptide-bond, carbonyl oxygen and amid (N+4))- rigid formation side chains extend outward
Beta sheet- parallel or anti parallel, H bond between peptide segments
Beta turns:
proline kink
Glycine packing
3:3-D arrangement of AA with linear peptide chain, protein folding patterns
4- multiple subunits
10
Q
what forms disulfide bond and what do disulfide bonds do?
where do these occur and under what conditions?
A
-2 cysteines
stabilize protein folds with crosslinks
oxidizing conditions in the ER or Golgi facilitate S-S formation
11
Q
Alzheimer’s Disease
Protein folds
A
Deposits of intracellular tau form neurofibrillary tangles; extracellular aggregates of amyloid-β form amyloid plaques.
12
Q
Parkinson’s disease
Protein folds
A
Formation of protein inclusion bodies (Lewy bodies) containing α-synuclein and ubiquitin.
13
Q
Huntington’s Disease
Protein folds
A
CAG (glutamine) repeat number correspond to the severity
Expansion of polyglutamine (pQ) results in intracellular aggregation of proteins.
14
Q
Amyotrophic Lateral Sclerosis (ALS)
Protein Folds
A
Formation of protein aggregates in motor neurons, associated with mutant superoxide dismutase proteins.
15
Q
Retinitis pigmentosa
protein golds
A
Accumulation of misfolded mutant rhodopsin inside endoplasmic reticulum of retinal cells
16
Q
Prion Protein (PrP)
A
causative agent of transmissible spongiform encephalopathies (TSEs), including Creutzfeldt-Jacob disease in humans, scrapie in sheep, and bovine spongiform encephalopathy in cattle.
17
Q
Hb vs Mb
which one follows allostery
A
Hb-quaternary structure of Hb uses cooperation to bind and unbind oxygen (allostery)
On the other hand Mb is hyperbolics (no cooperativity, follows MM kinetics)
18
Q
Collagen structure
A
long, rigid, 3 left handed- alpha helices wind forming triple helix
can form gel or strong fiber
rich in Pro and Gly
Small insertions of bulky groups into the alpha helices can dramatically modify the triple helix arrangement. Additional rigidity is created through cross-linking the chain together in a vitamin C dependent process.
19
Q
Collagen formation
A
- Pro and Lys side chains are hydroxylated during biosynthesis
- α chains assemble through initial formation of disulfide chains at C-terminus to enable triple helix formation.
- Procollagen is secreted into extracellular matrix.
- Terminal polypeptides are cleaved in extracellular space to form triple-helical tropocollagen.
- Collagen is cross-linked via lysyl oxidase, creating a strong fiber.
20
Q
Collagen diseases
A
EDS- stretchy skin, unable to process collagen correctly, mutations in AA sequences of 1,3,5
Osteogenesis imperfecta- brittle bones, results from reduced abundance of fibril forming collagen chains or mutations that interfere with helical packing.
21
Q
Osteogenesis imperfecta types
A
1: early infancy
2: in utero (prevents helix formation by replacing gly with bulky side chain)
22
Q
Elastin locations
A
Connective tissue protein in lungs, wall of large arteries, and elastic ligaments
degradation of elastin is required for tissue remodeling
23
Q
Elastin related diseases
A
Marfan syndrome (mutations in fibrillin-1 protein results in impaired structural integrity in skeleton, eye, and cardiovascular system)
Emphysema
Elastase degrades elastin in alveolar walls, and other structural proteins.
α1-antitrypsin (serpin superfamily) is a serine protease inhibitor that protects tissues from proteases released by inflammatory cells (e.g., neutrophil elastase).
24
Q
how smoking damages elastin
A
Smoking oxidizes methionines in α1-antitrypsin, inactivating this protease inhibitor causing elastase activity and lung damage (cleavage of elastin).
25
non polar
no O or N, oily
| more likely to face interior or a protein facing towards the outside of a trans membrane sequence
26
do polar side chains enhance or decrease water solubility
enhance
27
2 common bio buffers
bicarb, phosphate
28
most fundamental properties of a molecule for drug action is
its acid and base properties
29
aspirin
| acidic or basic
acidic
30
pyrimethamine
| acidic or basic
basic
31
beta turns involve which AAs
proline and glycine
32
peptide bonds form through what type of rxn
condenstion
33
tissue remodeling
requires elastin degredation, mediated by protease elastase
Elastase activity is tightly controlled by alpha1-antitrypsin (a serpin). Smoking oxidizes methionine in alpha1-antrypsin, resulting in activation of elastase and lung damage (major cause of emphysema).
34
lys involvement in elastin formation
Lys side-chains in tropoelastin are oxidatively deaminated to enable cross-linking of the chains to form elastin.
35
Prion proteins
Prion protein adopts infectious structure and represents the first identified infectious disease that only involve protein. Prion protein in the noninfectious state contains largely alpha helices. In contrast, the infectious form contains beta sheet structures.
36
Histones
and Histone core structure
Histones- basic AAs, proteins which interact with negatively charged DNA, DNA wraps around this
Histone core: 145 bp DNA and octamer of histones
37
Heterochromatin
very condensed, usually at centromeric and telomeric regions
38
Euchromatin
less condensed
39
Nucleosome core particle
DNA and octamer of 8 protein subunits
40
Epigenetic regulation
- control of gene expression by histone modification and modification of DNA bases but NOT the sequences (epigenetic- “on top of DNA modifications”)
41
subunits of core nucleosome particles
H2A with H2B 2 seperate, link with H3H4 tetramer (see pic)
42
Chromatin structure during Mitosis vs Interphase
Mitosis- chromosomes are condenses
| Interphase (G1, S, and G2)- chromosomes are decondensed, euchromatin, available for transcription and translation
43
chromosome nomenclature
6p21.34
```
6-chromosome number
p-short arm
2-region
1-sub region
3-sub-band
4- sub-sub band
```
44
histone modification
| acetylation on lysine
removes a positive charge on histones, may loosen interaction with DNA converted to more assessible
45
histone modification
| methylation occurs on lysine
mono, di, or tri, attract heterochromatin specific protein and strength interaction with DNA
46
histone modification
| phosphorylation on serine
adds negative charge to serine, reduces interaction from DNA and histones
47
effect of methylation on DNA
methylation of cytosines in CpG turns off the promoter
| -more methylation in inactive chromatin
48
enzymes that control acetylation and methylation on histones
– Histone acetyl - transferases (HATs) add acetyl group
– HDACs (histone deacetylase complexes) remove acetyl group
– Histone methyl transferases add methyl group
– Histone demethylases remove methyl group
49
gene expression
Expression of a small fraction of genes depends on their origin: paternal origin or maternal origin.
One of the two alleles (maternal or paternal) is expressed, and the other allele is imprinted (inactive or not expressed).
Imprinted genes are not expressed. Imprinted may be in heterochromatin state
50
relationship between Prader-Willi syndrome (PWS) and Angelman Syndrome (AS)
AS and PWS- deletions in chromosome 15q11-q13
| Two different syndromes but same deletion (depends on deletion from mother or father, parent specific inheritance)
51
Angelman Syndrome (AS)
```
• UBE3A
– E3 ubiquitin ligase
– Brain specific expression
– Maternally expressed
• Mutations in UBE3A gene are seen in AS individuals where maternal chromosome is not deleted
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52
Prader-Willi syndrome (PWS)
```
• Genes
– Multiple genes in the PWS region
• Approximately 20 paternally expressed genes are missing
– No mutations characterized
– Some candidate genes
• Necdin (NDN)
• SNURF-SNRPN
• snoRNAs
• Imprinting center
```
53
is warfarin dosing dependent on genotype?
yes, CYP (cytochrome p450) enzymes involve activation/inactivation of drugs
Warfarin dosing is depending on genotype isoforms of CYP enzymes of patient
54
history of determining DNA
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Mendel- unit factors genes
Griffith’s experiments- virulent strain vs avirulent strain and mice, helped determine DNA had genes
Bacteriophages inject DNA
Chargaff’s rules- A=T, C=G
Watson and Crick Model
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55
ribose vs deoxyribose
sugar w/wo O
56
Purines
AG
57
Pyrimidines
CUT
58
Nucleotide
Nucleoside + phosphate, make up back bone
59
Nucleotide uses
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DNA/RNA constituents, Cofactors,
energy currency (ATP),
cell signaling (GTP in G protein couple receptor)
```
More examples: FAD, NAD (electron carriers), cAMP, cGMP (2nd messengers), CoA (carbon carrier in FA metabolism)
60
analogs of base, nucleoside, and nucleotide therapeutic agents
– Base analog
5-fluorouracil (cancer therapeutic)
– Nucleoside analogs
Ganciclovir: 2’ deoxy guanosine analog (CMV retinitis therapy)
AZT (Zidovudine): 3’-deoxy-3’-azido-thymidine (HIV/AIDS)
– Nucleotide analog
Adefovir (Hepatitis)
61
distinct structural features, strand orientation and complementarity in DNA
Antiparallel strands, B 10 bases/turn, right handed turn= for humans
62
DNA denaturation kinetics
concentration indepenent
63
DNA renaturation
2nd order kinetics, dependent on concentration of strands
64
distinction between hyperchromicity of single and double stranded DNA and its application for determining base composition
Double stranded= S shaped curve because CG bonds are stronger
Single stranded= linear
65
non watson-crick basepairing
Non WC- can stabilize some single stranded conformation, used in gene regulation and telomere stability
66
I-motifs (intercalated motif)-
found in C rish regions of the genome at telomeres and promoters, they are formed between protonated C and neutral C in a single strand of a double stranded DNS
I motifs help visualize structures, vary with cell cycle phases
67
Effects of alkylating agents such as cyclophosamide, nirosourea and cisplatin on DNA structure and their utility for therapy
DNA = damaged by alkylation
| cyclophosamide, nirosourea and cisplatin, chemo drugs that cause cell death
68
start codon
AUG (met)
69
stop codon
UAG, UGA, UAA
70
Protein vs enzyme
Enzymes are a group of proteins that catalyze chemical transformations
Proteins can be involved in:
catalysis/chemical transformation- phosphofructokinase, polymerases
Extracellular signaling (insulin, glucagon, anfiotensin)
Cell structure (actin, tublin)
Transport (hemoglobin, albumin)
Energy transduction (ion transport, muscle contraction)
Immunity (antibodies)
71
Oxidoreductases
catalyze oxidation/reduction reactions that typically involve electron transfer involving NAD(P)+/NAD(P)H or FAD/FADH2
• NADH is electron donor, pyruvate is electron acceptor
• NAD(P)+ + 2e- NAD(P)H
(Mobile Electron Carrier)
• FAD/FMN is a 2 e- oxidizing agent, which becomes reduced to FADH2/FMNH2
These rxns are important in cytochrome P450 (CYP) in oxidative metabolism
72
Transferases
catalyze transfer of C-, N-, or P-containing groups
•Ex aspartate amino transferase
•Hexokinase
73
Hydrolases
catalyze cleavage of bonds by addition of water
| • Ribonuclease (RNase), Phosphodiesterase
74
Lyases
catalyze cleavage of carbon-carbon, carbon-sulfur, and carbon-nitrogen bonds
75
Isomerases
catalyze racemization of optical or geometric isomers (no net change in bonding)
76
Ligases
catalyze the formation of bonds between carbon and oxygen, sulfur, or nitrogen coupled with input of energy (typically involving ATP).
77
functional significance of a zymogen (proenzyme) in terms of the need to deliver proteases to proper compartment (extracellular matrix or plasma) prior to enzyme activation.
Zymogens are inactive and they prevent enzyme action in unwanted locations
Protease activation occurs after extracellular transport
78
apoenzyme
| active or inacive
inactive
79
Holoenzyme
apoenzyme + cofactor
80
isoenzymes
represent important biomarkers for dx
Ex: level of CK type in different tissues
Skeletal M, cardiac MB, brain B
Elevated CK can diagnose MI, skeletal muscle diseases (muscular dystrophy)
81
to describe the different roles of the protein side chains within an enzyme active site in terms of binding and catalysis, and relationships to pH optimum.
Active site: substrate binds to enzyme active site where substrate is chemically transformed into product
Binding interactions: temporary bonds form with substrate in binding site
Catalysis involves distinct side chains: catalytic side chains medicate chemistry
82
post-translational protein modifications (PTMs)
Protein phosphorylation (Tyr, Ser, Thr); global regulation of cell function
Glycosylation of extracellular proteins permit self-recognition
Ubiquitination and SUMOylation and respective involvement in protein degradation or protein localization and binding interactions
Oxidation/Reduction and role of disulfide bond formation in the stabilization of protein structure)
Acetylation and regulation of DNA packaging in histone complexes to regulate transcription (formation of mRNA)
Lipidation and membrane targeting
Methylation and mediation of protein recognition or modulation of other PTMs.
83
Thiamin Pyrophoasphate (TPP) as a cofactor
co factor of oxidative decaboxylase
ex pyruvate to acetyl CoA
84
FAD/FADH2 as a cofactor
oxidation/reducation, serves in electron storage, often couples with NAD+
85
NAD(P)+/NAD(P)H as a cofactor
redox rxn, mobile electron carrier
86
CoA-SH as a cofactor
acyl group transfer
87
Pyridoxal Phosphate (PLP) as a cofactor
catalyzes transamination, deamination, and decarboxylation reations
involved in AA metabolism
88
Biotin as a cofactor
```
carboxylation reactions (Carries Activated CO2)
Pyruvate to oxaloacetate
```
89
tetrahydrofolate
transfer one carbon fragments
methylation of homocysteine to form methionine
90
Semiconservative
1 old and 1 new strand when replicated
91
Okazaki fragments
on lagging strand
bacterial okazaki fragments- 1.0 to 2.0 Kb
Human o frag- 0.1 to 0.2 Kb
92
Proof reading
DNA polymerase can edit and proofread to reduce error rate
93
Helicase
unwinds to strands
94
Primase
in bacteria synthesizes RNA primers
95
Polymerase a
in humans synthesizes RNA primers
96
DNA polymerase III (replicase)
in bacteria adds new nucleotides to the 3’
97
Polyemerase e and d
adds new nucleotides to the 3’
| in humans
98
DNA polyermase I
in bacteria- removes primers
99
RNaseH
removes primers in humans (mutations in this cause neuro- inflammatory disorders and in systemic lupus)
100
DNA ligase
joins fragments
101
Type II topoisomerase (Gyrase in E coli)-
relieves unwinding, cuts both strands and allows DNA to rotate, heterotetromer (A2B2)
Type 1- makes nicks on 1 strand
Type II (bacterial DNA gyrase)- makes 2 guts
102
DNA polymerase bacteria
Bacteria (multisubunit)
Polymerase Activities
Pol I 5’-3’ polymerization
5’-3’ exonuclease
3’-5’ exonuclease
Pol II 5’-3’ polymerization
3’-5’ exonuclease
```
Pol III (replicase) 5’-3’ polymerization
3’-5’ exonuclease
```
Bacterial initiation protein
1 origin of insertion
103
Human polymerase bacteria
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Human (multisubunits)- editing and proof reding
Polymerase a (primase)
Polymerase b (repair)
Polymerase g (mitochondrial replication)
Polymerase d (nuclear replication)
Polymerase e (nuclear replication)
```
Thousands of origins of replication
104
gyrase
Point mutations in gyrase lead to antibiotic resistance:
N-terminal end of GyrA (most mutations).
C-terminal end of GyrB (few mutations).
105
Replication inhibition in cancers
Mammalian Topo I is the target enzyme for anticancer drugs
Topoisomerase I makes a cut on one strand of the DNA and binds to 3’ end of the phosphodiester back bone
After it relieves the supercoiling, DNA is religated
Topotecan (Hycamtin) is FDA approved for ovarian cancer and small cell lung cancer
Topotecan stabilizes Topo I-DNA complex and prevents the religation step (inhibition of replication)
106
End replication problem
E. coli has circular genome: replication starts at origin and proceeds around the circle to completion
In linear mammalian chromosomes, when replication fork reaches the end, RNA primer can’t be placed for the last Okazaki fragment
Once the RNA primer is removed from the 5’ end, it cannot be filled up.
No polymerase available with 3’-5’ activity
5’ ends will shorten after each replication cycle
What will be the consequences?
Coding sequences may be eventually lost
Senescence or death signal may be triggered
Does not occur in circular, bacteria, DNA
107
Telomeres
seal the end of chromosomes to prevent undesirable fusion and aberrant recombination, attach chromosomes to nuclear envelope, facilitate replication
108
Telomerase
RNA dependent DNA polymerase (reverse transcriptase), made of ribonucleoprotein and RNA, makes telomeric repeats
Telomeric repeats humans TTAGGG (up to 15 Kb)
109
telomeres and aging
```
shorter telomeres induce replicative senescence and induce cell death
Somatic cells (differentiated)- no detectable telomerase activity
Germ cells and stem cells- have detectable activity
Elderly have shorter fibroblast telomeres
```
110
telomeres and cancer
tumors have telomerase activity, inhibition or activity or disrupting structures would prevent tumor growth (effective in mice)
Germ cells also have telomerase activity
-therapeutic agents can inhibit nucleotide synthesis
Ex: thymidylate synthase (TS) converts dUMP to dTMP
5-Flurouracil inhibrits TS (Capecitabine (Xeloda)- chemo agent)
111
AZT as a therapy for HIV replication
HIV- RNA virus, requires RNA DNA, priming tRNA (tRNA-lys), cDNA formation by reverse transcriptase, then inserts into host genome by integrase
Targets for inhibition- replication, integrase, protease
Ex: AZT- analog for deoxythymidine, this prevents DNA chain elongation by reverse transcriptase
112
Role thymidylate synthase in replication, and mechanism of 5-fluoro uracil as chemotherapeutic agent
therapeutic agents can inhibit nucleotide synthesis
Ex: thymidylate synthase (TS) converts dUMP to dTMP
5-Flurouracil inhibrits TS (Capecitabine (Xeloda)- chemo agent)
113
Mismatch repair
wrong base pairing (methylated at the mistakes)
In bacteria Mut S, L, H
In Euks Mut S- recognizes mismatch, Mut L scans for nicks
114
Depurination
removes purine from nucleotide, leads to baseless sugar- P, consequences: leads to deletion
115
Deamination
methylated cytosine to thymine, C U, consequences: changes base
116
UV- consequences:
creates pyrimidine dimers form
117
replication repairs
3’ to 5’ exonuclease activity, removes mismatched nucleotide
| Also stranded-directed mismatch repair when DNA helix is altered
118
post-replication repairs
```
including transitions, transversions, frameshifts)
Purpose is to correct mismatched basepair
In E coli- methylation
In Euks- single strand breaks, nicks
Errors may occur due to:
Structural alterations in DNA bases may occur due to:
Cellular metabolic activity
Heat
Extreme pH
Radiations
Substances in environment
Spontaneous Changes:
Depurination
Deamination
UV damage
Pyrimidine dimers
```
119
lynch syndrome
mismatch repair
hereditary non-polyposis colon cancer (HNPCC)
Mutations in human homologs of mutS (MSH2) and mutL (MLH1) are involved.
120
BER
specific base removed and repaired, (ex. Uracil DNA Glycosylase)
121
NER
stretch of DNA strand is removed and new strand with correct base is made (ex excision nuclease)
122
missmatch repair
repair of non-Watson-crick basepairs
123
double stranded break
see photo
```
Double strand breaks occur during:
Recombination (RAG-recombination activating gene-proteins catalyzing recombination of immunoglobulins)
Ionizing radiation, oxidizing agents
Double strand breaks are repaired by:
Non-homologous end-joining (NHEJ)
Involves Ku protein, DNA-PK and Artemis
Homologous end-joining (HEJ)
Involves BRCA1 and BRCA2
```
124
repair defect cause diseases
```
Xeroderma pigmentosum (XP)
Skin malignancies
```
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Cockayne syndrome (CS)-ERCC6/ERCC8 mutation
Premature aging, photosensitivity, hearing loss etc.
```
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Breast cancer (BRCA1 and BRCA2)
17q21 and 13q12
```
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Werner syndrome (WRN RecQ helicase mutation-helicase/exonuclease activity)
Cataracts, short stature, premature graying etc
```
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Bloom syndrome (BLM RecQ helicase mutation-helicase activity only)
Stunted growth sunlight sensitivity, chromosome breakage, increased cancer risk etc.
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125
Transition state theroy
activation barrier to binding the substrate, but once bound that activation barrier is lower, making the reaction more likely and the rate of reaction increases. It is the reduction in the activation barrier, and not the chemical potential, that increases the rate of reaction.
126
allosteric enzymes
multiple subunits
bind far from active side
S shaped sigmoidal substrate-velocity relationship
large change in activity over a narrow range of substrate concentrations
127
Michaelis-Menton
hyperbolic substrate velocity relationship
128
know inhibitor graphs and ES thing
know enzyme graphs`
129
regulatory mechanisms to modify enzymes
* Substrate concentrations
* Allosteric regulators
* Post-translational modifications (e.g., phosphorylation)
* Abundance (i.e., translation/transcription or proteolysis)
130
competitive inhibitor
Vmax- no change
| Km- increases
131
noncompetitive inhibitor
Vmax- decreases
| Km- no change
132
uncompetitive (mixed) inhibitor
Vmax- decreases
| Km- decreases
133
competitive inhibitor examples
- statins (HMG-CoA reductase)
- methyltrexate (dihydrofolate reductase)
- Salicylate (cyclooxygenase 2, COX 2)
134
noncompetitive inhibitor examples
- cynaide (cytochromes)
- D-JNKI-1
- Nifedipine (CYP2C9)
135
uncompetitive (mixed) inhibitor examples
- pepstatin
- trypsin inhibtor (trypsin)
- ethanol (acid phosphatase)
136
irreversible inhibitors
example: aspirin
Aspirin covalently modifies COX-1 and COX-2 by acylation of Ser near active site (blocks prostaglandin biosynthesis).
```
Advantages of covalent drugs include:
Selectivity
Lower doses and side effects
Prolonged duration of inhibition
Lower risk of drug resistance due to active site residue changes
```
Covalent drugs target more than 39 enzyme targets include:
H+/K+ ATPase (gastric acid)
β-lactamases (antibiotic detoxification)
137
enzyme regulatory mechanisms
* Allosteric Effectors (e.g., fructose-2-phosphate); Very Fast
* Post-translational Modifications (e.g., enzyme phosphorylation); Fast
* Enzyme Abundance (transcriptional regulation); Slow
138
Zygote
fertilized egg, after nuclear fusion
139
pre-implantation stages
first 2 weeks, zygote; 2-8 cell stages morala, blastocyst, bilaminar disc
140
embryo
developing organism from 2-8 wks EDF
141
fetus
developing organism from 9 wks to birth EDF
142
trimester
1/3 of the human gestational periods, not related to developmental stages
143
growth
Increase in cell number, cell size, and extracellular matrix
144
differential growth
one side or part of a structure grows faster than another
145
induction
a chemical signal (surface signaling molecule or chemical released into extracellular matrix) will cause a change in cells resulting in migration differentiation or other change
146
cell differentiation
nonspecialized to specialized cells, some genes are activated (determination), others inactivated (restriction), usually permanent, metaplasia (pathologic de/re differentiation)
147
Selective cell death
cells are programed to die for structure to develop normally, example hand cells between fingers die and brain large number of cells die in fetal life
148
migration
physical movement of cells from one location to another, usually involves amoeboid movement and chemotaxis
149
epithelial folding
upon appropriate induction, the edges of some type of poorly differentiated, flat epithelia can fold over on themselves to form a tube, example neural tube with actin filaments
150
cavitation/canalization
opening of spaces in originally solid tissues as the cells move to a peripheral location
151
morphogens
Diffusible molecules that create gradients which act directly on cells for specific developmental responses.
152
notch signaling pathway
conserved intercellular signaling pathway using direct cell-to-cell contact.
153
transcription factors
Binds to DNA, initiates transcription of mRNA. Many are Homeobox or HLH families.
154
receptor tyrosine kinsases
Cell-surface receptors, includes growth factors which regulate cell migration, proliferation, and apoptosis, new growth, etc. (also in normal cells, where they involve cytokines and hormone receptors)
155
important classes of developmental factors commonly involved in human development (4)
- morphogens
- notch signaling pathyway
- transcription factors
- receptor tyrosine kinases
156
Meiosis
chromosomes 1 DNA replication, 2 divisions(4n to 2n (2 copies of 23 chromosomes) to n)
Gametogonium- 46 replicated chromosomes, divides by standard mitosis, daughter calls may differentiate into primary gametocytes
Gameotyocytes- 46 chromosomes which line up in homologous pairs (4n), divides in division I to form secondary gametocytes with 23 replicated chromosomes (2n)
Division II to form two gametes a piece (4 total) each with 23 nonreplicatd chromosomes (n)
157
mitosis
All cells
1 DNA replication, 1 division (4n to 2n( 46 complete chromosomes)
IPMAT
158
Spermatogenesis:
Spermatogonia undergo mitosis
Primary and secondary spermatocytes undergo meiosis
Spermiogenesis is the morphological differentiation of spermatids into spermatozoa.
159
Oogenisis:
Primary oocyte 46, xx
Secondary oocyte 23, x a primary oocyte also forms a polar body to get rid of secondary DNA
Ovum 23, x meets with sperm 23 x or y
Zygote 46, XY or XX
160
transcription growth factor beta (TGF-b)
example of morphogen
promotes cell growth and differentiation; uses SMAD pathway. Think angiogenesis, Mesoderm migration, Axons.
161
Bone Morphogenic Proteins (BMP’s):
one of the pivotal developmental signaling molecules; think cell differentiation.
162
Hedgehog series: (e.g. SHH)
critical developmental gene requires cholesterol to become active. SHH; think development of vertebrae, paraxial mesoderm.
163
WNT (Wingless-related integration site):
Critical in pattern development and axis patterning among other things, it uses β-catenin to activate gene sequences. Think muscle development.
