Biology Lectures 1St Semester

Front 1

centrosome

Back 1

created out of 2 centroiles

replicated during G1

make the microtubules

Front 2

gradietn centrifuge

Back 2

organelles seperation according to sizeq

Front 3

prokryotic cytoskeleton

Back 3

actin-tubulin

Front 4

eukaryotic ribisome size

Back 4

80S

Front 5

prokaryotic ribosome size

Back 5

70S

Front 6

what is protozoa

Back 6

eukaryotic multicellular

(malaria, leishmania)

Front 7

methylgreen

Back 7

DNA specific (=purple DNA)

Front 8

pyronine

Back 8

RNA specific (=pink cytosole)

Front 9

morbus gaucher

Back 9

lysosomal disease (increased liver+spleen+osteolysis)

Front 10

peroxisome

Back 10

unilayer bound,

calayze peroxide (convert it into water)

detoxify alcohol+ bile acid+ fats

Front 11

zellweger syndrome

Back 11

malfunction perioxisome

psychomotoric retardation

Front 12

dynein

Back 12

takes chromsome from + (center cell)-> to - (centrosome)

Front 13

kinesin

Back 13

goes from - (centrosome)-> to + (center)

Front 14

thickness of lipid monolayer

Back 14

100micrometer

Front 15

movement of PL in the membrane

Back 15

1. rotation (turns around itself)

2. lateral migration (moves in the same layer)

3. flip-flop\ transverse (moves to the other layer)

Front 16

what can pass through membrane

Back 16

1. small hydrophobic (o2, co2, n2, benzene)

2. small uncharged polar (H2o, glycerol, ethanol)

Front 17

what can't pass through membrane

Back 17

1. larger uncharged polar (aa, glucose, nucleotide)

2. ions ( H+, Na+, HCO3-, K+, Ca+2, Cl-, Mg+2)

Front 18

uniport

Back 18

passes one thing across membrane

Front 19

symport

Back 19

coupled with antiport

passes 2 things across membrane

Front 20

antiport

Back 20

coupled with symport

passed 2 thing across membrane (one in, one out)

Front 21

osteogenesis imperfecta

Back 21

disorder of the bone development

due to mutation in the collagen genes

Front 22

Ehlers Danlos syndrome

Back 22

malassembly of collagen

hyperelaticity

Front 23

marfan syndrome

Back 23

dominant

causes long limbs and fingers

thin aorta wall

due to mutation in genes for elastinb

Front 24

glycosaminoglycans (GAG)

Back 24

hyaluron, chondroitin, sulphate, heparan sulphate

fill space btw collagen fibers

Front 25

proteoglycans

Back 25

GAG+ core protein

have a role in signaling, (bind\block growth factors)

Front 26

alport syndrome

Back 26

mutation in collagene gene,

leads to dysfunction glomerular filter

Front 27

goodposture synteume

Back 27

antibodies attack the basal lamina

Front 28

width of IM filaments

Back 28

10nm

Front 29

width of microtubules

Back 29

25nm

Front 30

width of actin filaments (microfilaments)

Back 30

7nm

Front 31

component of microfilament

Back 31

globular G actin

Front 32

component of microtubule

Back 32

globular tubulin alpha+beta

Front 33

components of IM filaments

Back 33

various proteins (keratin, vimetin, desmin)

Front 34

what cytoskeleton form is unique for animal cells

Back 34

the IM filaments

Front 35

protein of anchodring adhesion

Back 35

cadherin

Front 36

protein of gap adesion

Back 36

connexin

Front 37

protein of tight adhesino

Back 37

occluding

Front 38

structure of IM filaments

Back 38

2 tetromer linked at their ends (2 dimers togheter) = protofilament

8 protofilament= single IM filament

Front 39

what kind of junction does IM filament make?

Back 39

desmosome (ancdhoring)

Front 40

structure of microtubule

Back 40

13 protofilaments (doubles of alpha+beta)

Front 41

side of growth of MT

Back 41

the one with GTP (on the + end)

Front 42

basal body structure

Back 42

of MT

9+0 triplets

is the "base" of the flagella+ cillia

reponsible for the movement

there are 9 triplets with nothing in the middle

Front 43

cillia and flagella

Back 43

are arranged in 9 doublets (9+2)

9 doublets around, and 2 in the middle

Front 44

strucutre of microfilaments

Back 44

2 chains of one microfilament= actin

with + and - ends

Front 45

wisdcott aldrich syndrome

Back 45

mutation in the WASP gene (descrease motility of lymph tissue) = slow immunocyte

Front 46

MPF

Back 46

CDC 2+ cyclin B

Front 47

G1 control

Back 47

CDK4\6+ cyclin D

Front 48

late G1 control

Back 48

CDK2+ cyclin E

Front 49

S phase contro

Back 49

CDK2+ cyclin A

Front 50

cyclin-CDK expression in cancer cells?

Back 50

overexpressed

Front 51

what degrgated the cyclin-CDK?

Back 51

Ubiquitin-> initiates the APC phase

Front 52

inhibitor to cell cycle (of growth)

Back 52

TGF-> (induces the) P15 (can be inhibitor\ stimuli)

Front 53

to initiate the anaphase

Back 53

the CDK-cyclin complex must be degraded

Front 54

what halts the APC checkpoint

Back 54

unattached chromsomes will keep the checkpoint "on" with mad+bob proteins into a complex blocking cdc to activate the APC

Front 55

size of cell nucleus

Back 55

5-10 micrometer

Front 56

layers of nucleus membrane

Back 56

outer

1. outher membrane

2. perinuclear space (20-40mn)

3. inner membrane

4. nuclear lamina

Front 57

diameter of nuclear pore

Back 57

120nm

Front 58

how many subunits is the nuclear pore is made of?

Back 58

8 subunits

Front 59

name of nuclear import receptors

Back 59

importins (recieves )

Front 60

receptor on molecule enables entry to the nucleus

Back 60

NLS (nuclear localization signal)

interacts with the importins of the nuclear pores

Front 61

name of nuclear export receptor

Back 61

exportins (pushes molecule outside)

Front 62

receptor on the molecule enables exit to the cytoplasma

Back 62

NES (nuclear export signal)

interacts with the exportins

Front 63

heterochromatin

Back 63

highly condensed

Front 64

euchroamtin

Back 64

decondensed, during interphase

Front 65

size of telomer

Back 65

TTAGGG in 2,000 copies

Front 66

parts of DNA enable to go through segregation

Back 66

1. telomeres

2. replication origin

3. centrome

Front 67

elongation of telomerase

Back 67

from the 5'-> 3'

Front 68

from what does the nuclear lamina made of?

Back 68

IM filaments ( lamina A, B, c)

Front 69

dyskertosis congenita

Back 69

premature telomer shortning

Front 70

to where does the chromosomes are attached to int he nucleus?

Back 70

the nuclear envelope

the nuclear lamina (via receptors)- LAP1-2, transcription factors RB, BAF, chromatin associated proteins (LBR)

Front 71

cajal bodies

Back 71

pre-mRNA splicing factor

Front 72

what do we have in the nucleolus?

Back 72

5 chromsome pair= 10 chromsomes

10 clusters of rRNA genes on the chromsomes

ribosomal subunits, rRNA prcosses rnzyme s

Front 73

pars fibroas of nucleolus

Back 73

newly synthesizes rRNA

Front 74

pars granulosa of nucleolus

Back 74

post rRNA transcription-> linked to other proteins la

Front 75

laminopathies

Back 75

rare, mutation in gene coding for the nuclear lamina

(progeria, dreifuss muscular dystrophy, partial lipdystrophy Dunning type)

Front 76

from which end does the mRNA enters the ribosome

Back 76

5'

Front 77

what is on the A area of ribosome

Back 77

bindig of aminoacyl-tRNA

Front 78

what is on the P area of ribosome

Back 78

binding of peptidyl- tRNA

Front 79

malfunction ribosome

Back 79

1. diamond black anemia

2. congenital X linked dyskeratosis

3. achwann diamond sydnroem

Front 80

parts of proteosoms

Back 80

20s+19s

Front 81

eukaryotic ribosome parts

Back 81

60s+40S

Front 82

autophagy

Back 82

by autolysosome by lysosome,

self digestion

Front 83

necrosis

Back 83

accidental cell death

Front 84

steps of apoptosis

Back 84

1. membrane blebbing (cytoskeleton break down and bulges)

2. chromatic condensation (brekaing chromsomes into fragmants)

3. cytoplamsic fragmentation (in mem. bound bodies)

4. fragmented (into apoptotic bodies with nucleus remnants

Front 85

ced3 mutation

Back 85

allows cells to live forever

Front 86

head of the apoptosis ligand

Back 86

caspases

Front 87

caspases cascade

Back 87

1. procaspases

2. activated and cleaved

3. activates more procaspases

4. explosive reaction

5. key proteins are cleaved

6. programmed cell death

Front 88

inhibitors of apoptosis

Back 88

IAP (clAP1-2)

Front 89

inhibitors of the inhibitoris of apoptosis

Back 89

diablo\smac (bind to IAP)

Front 90

types of apoptotic pathways

Back 90

1. intrinsic

2. extrinsic

Front 91

intrinsic apoptotic pathway

Back 91

1. from mitochondria

2. release of cytochrome C

3. release proapoptotic factors

4. cytorchome C causes aggreg. of -> apaf 1

5. apaf 1-> procaspases 9

6. caspase cascade

Front 92

intrinsic apoptotic pathway

Back 92

1. ligand attached to death receptors (TNF)

2. FASS in cytoplasm is activated

3. DISC complex is formed

4. caspases 8+10 is activated

5. converted into intrinsitc pathway

Front 93

substrates of caspases

Back 93

1. structural proteins (lamins, keratin 18 (IM fil. , actine fil.)

2. signal proteins (cPLA2, PKC, Bcl-2)

3. transcriptional factors (RB, MDM2, CAD)

Front 94

stuff released from mitochondria during intrinsic apoptotsis

Back 94

1. bcl-2 (bid, bak, bax) (proapoptotic)

2. cytochrome

3. smac\diablo (inactivates IAP)-> activates caspases)

Front 95

epigenetic regulation

Back 95

1. methylation of a DNA (silencing)

2. chromatin remodeling

3. tryptophan transcription

4. LaxZYA transcription

Front 96

rett sydnrome

Back 96

attachment ot methylacetsin to a protein-> mutatio in MECP2 gene (gene takes part in silencing genes)

on the X chromoromse, 95% occurs from sperm

= inability to shut down specific genes

Front 97

high enviroemntm tryptophan

Back 97

1. Trp binds to suppressor

2. supressor activated

3. binds to gene

4. diabales transcription

Front 98

no tryptophan in environemnent

Back 98

1. supressor is silent

2. RNA pol. binds to gene and transcribes

Front 99

low glucose in lacYA gene

Back 99

high Camp

Front 100

high lactose+ no glucose

Back 100

transcription

Front 101

promotor

Back 101

DNA initiation of transcription (RNA pol.)

Front 102

operator

Back 102

in the promotor

binding site for suppressor

Front 103

repressor

Back 103

negative regualtion

Front 104

+gucose

- lactose

Back 104

repressor binds to operator = no transcription

Front 105

glucose-

lactose+

Back 105

high cAMP binds to promotor = increase the affinity of RNA pol. to it= enables transcriptions

Front 106

eukaryotic genetic organization

Back 106

monocistronic

Front 107

prokaryotic

Back 107

polycystronic

Front 108

eukaryotic untranslated DNA part

Back 108

95%

Front 109

TATA box

Back 109

part of promotor

Front 110

microRNA

Back 110

regulate expression of genes,

bind to 3' untranslated part of mRNA