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Cell Biology > 1. Termin > Flashcards

1. Termin Flashcards

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1
Q

During the post translocation of proteins across the plasma membrane of bacteria SecA is directly involved in
- the recognition of the signal sequence
- the transport of the polypeptide chain through the SecYEG channel
- the cleavage of the signal sequence

A

the transport of the polypeptide chain through the SecYEG channel

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2
Q

SecA needs for its activity the presence of
- ATP
- GTP
- PMF

A

ATP

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3
Q

YidC is supporting the integration of membrane proteins into the bacterial plasma membrane
- in cooperation with the SecYEG-complex
- as the only directly involved membrane protein
- only during the integration of potassium sensors

A
  • in cooperation with the SecYEG-complex
  • as the only directly involved membrane protein
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4
Q

Proteins homologous to the YidC are present in
- plastids
- peroxisomes
- lysosomes

A

plastids

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5
Q

Proteins of the outer membrane of proteobacteria
- can be anchored by lipids
- usually acquire their transmembrane topology in the inner membrane via SecYEG and are subsequently sorted to the outer membrane
- are usually anchored via alpha-helical peptide elements

A

can be anchored by lipids

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6
Q

The disposal of misfiled proteins of the bacterial periplasma usually occurs
- via back-translocation into the cytoplasm
- with the help of proteases located in the periplasma
- via secretion of these proteins into the extracellular space

A

with the help of proteases located In the periplasma

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7
Q

The biogenesis of beta-barrel proteins in mitochondria requires
- TOM-complexes
- chaperoning protein complexes of the inter membrane space
- TIM17

A
  • TOM-complexes
  • chaperoning protein complexes of the inter membrane space
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8
Q

Membrane proteins of the outer mitochondrial membrane anchored by an alpha-helical membrane-spanning segment
- are always tail-anchored proteins
- may be integrated employing the TOM-complex
- do not exist, since all outer membrane proteins of mitochondria are anchored by beta-barrels

A

may be integrated employing the TOM-complex

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9
Q

The TIM23-complex
- translocates proteins via the inner membrane into the matrix
- Supports the integration of single-spanning membrane proteins into the inner membrane
- makes transient contacts to the TOM-complex

A
  • translocates proteins via the inner membrane into the matrix
  • Supports the integration of single-spanning membrane proteins into the inner membrane
  • makes transient contacts to the TOM-complex
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10
Q

Carrier proteins of the inner mitochondrial membrane use
- cleavable matrix targeting sequences
- hydrophobic alpha-helical segments
- internal acidic segments
as topogenic signals.

A

hydrophobic alpha-helical segments

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11
Q

Name three properties that distinguish a “complex plastid” from a normal chloroplast

A
  • mehrere Genome
  • mehrere Membranen müssen durchquert werden
  • mehrere Endosymbiontenereignisse
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12
Q

Describe the “cisternal maturation” model of the intra-Golgi transport. Focus on processes in the early Golgi using terms ER, vesicle, COPI, ERGIC, cis-Golgi, medial Golgi, membrane proteins

A

The cisternal maturation model is a hypothesis about how the Golgi apparatus works. It posits that secretory cargo travel in cisternal compartments that slowly mature from the cis-Golgi to the trans-Golgi composition. This is driven by three processes.
(1) New cis-cisternae are created by the homotypic fusion of ER-derived COPII vesicles at the ER-Golgi intermediate compartment (ERGIC).
(2) Old trans-cisternae dissipate by the vesiculation of the trans-Golgi network (TGN) into Golgi-to-surface carriers.
(3) Golgi-resident proteins are recycled along retrograde vesicles, including COPI vesicles, moving from older to younger cisternae.
Similar processes govern the maturation of endosomes in the endocytic pathway.

Cisternal maturation allows cells to process and secrete large cargo

Though we refer to vesicle transport throughout the text, our Boolean framework can also accommodate non-vesicular pathways. Some types of molecular labels can exchange between compartments only via transport vesicles. These include most lipids, and transmembrane proteins such as receptors and SNAREs.

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13
Q

The import of proteins into the storm of plastids occurs usually
- across porin-like channels in the outer plastid membrane
- via the membrane protein complexes TOC and TIC
- with the help of transport vesicles

A

via the membrane protein complexes TOC and TIC

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14
Q

The import of proteins into the peroxisomal matrix
- requires always a complete unfolding of the substrate proteins
- requires ubiquitin
- is driven by an electrochemical potential at the peroxisomal membrane

A

requires ubiquitin

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15
Q

Name three organelles, which can be a source of exocytotic vesicles or which can undergo exocytosis themselves

A
  • Lysosomen/lysosomal bodies
    -> multi vesicular bodies
  • recycling endosome
  • secreting lysosomes
  • autolysosomes
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16
Q

Secretory granules form at
- the TGN
- early endosomes
- the ER

A

the TGN

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17
Q

Clostridial neurotoxins
- are proteases cleaving SNARE proteins involved in the exocytosis of synaptic vesicles
- are inhibitors which block the recycling of SNAREs from the plasma membrane to synaptic vesicles
- are inhibitors, which block the closing of the fusion pore

A

are proteases cleaving SNARE proteins involved in the exocytosis of synaptic vesicles

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18
Q

The formation of clathrate-coated pits is induced by
- the formation of phosphatidyl-inositol 4,5 phosphate
- the presence of multiubiquitinylated membrane proteins
- the influx of calcium ions

A
  • the formation of phosphatidyl-inositol 4,5 phosphate
  • the presence of multiubiquitininylated membrane proteins
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19
Q

The sorting of proteins into internal vesicles of MVBs needs the activity of
- COPI
- ESCRTIII
- caveolin

A

ESCRTIII

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20
Q

Endocytotic Cathrin-coated vesicles
- may take up virus particles
- are pinched off from the plasma membrane by Dynamin
- contain AP4 as a coat component

A
  • may take up virus particles
  • are pinched off from the plasma membrane by Dynamin
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21
Q

During transition from early to late endosomes (= Endosomal maturation)
- vesicles are delivered towards the TGN
- the luminal pH is increasing
- internal vesicles in the endosome are formed

A
  • vesicles are delivered towards the TGN
  • internal vesicles in the endosome are formed
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22
Q

Melanosomes arise from
- early endosomes
- cis-Golgi stacks
- phagolysosomes

A

early endosomes

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23
Q

Exosomes are released by
- a process similar to the budding of viruses from the plasma membrane
- exocytosis of MVB
- exocytosis of autophagolysosomes

A

exocytosis of MVB

24
Q

Lipid droplets
- are formed at the ER
- are the main storage compartment for glycosphingolipids
- form contact sites with membranes of different organelles

A
  • are formed at the ER
  • form contact sites with membranes of different organelles
25
Q

Name two mechanisms, which allow the degradation of biological membrane in the lumen of the lysosome. Which property protects the limiting membrane against a possible self-digestion?

A
  • endocytosis, phagocytosis, autophagy
    1) LAMP
    2) glycosylation - glycoproteins
    3) LBPA
26
Q

Name two pathways for the transport of lipids from the ER to the TGN

A

1) Vesikulärer (sekretorischer) Weg
2) ER-TGN Kontaktstellen

27
Q

The division of mitochondria
- involves GTPases
- results in a short-term mixing of the outer and the inner mitochondrial membrane
- is also occurring in the S-phase

A
  • involves GTPases
  • is also occurring in the S-phase
28
Q

During cytokinesis the ER of somatic mammalian cells is generally
- vesicular
- tubular
- sheet-like

A

tubular

29
Q

The fusion of mammalian somatic cells
- is only observed ex vivo under laboratory conditions
- uses proteins homologous to SNAREs as fusogene
- is in vivo only observed during early embryogenesis

A

NONE

30
Q

The morphology of the ER network is controlled by
- proteins that induce curvature of the ER-membrane
- proteins, that stabilize three way junctions
- myosin motors linked to intermediate filaments

A
  • proteins that induce curvature of the ER-membrane
  • proteins, that stabilize three way junctions
31
Q

Is polyadenylation for all mRNAs a stabilizing motif? Justify your statement.

A

Nein, denn in Prokaryonten ist Polyadenlyierung ein Signal für den Abbau.

32
Q

The cellular m:R-l22 is a critical host factor for the Hepatitis C Virus life <ycle. Which of the statements Goncerning the mechanisti< and/or functional features for miR-I22’s role in the HCV life cycle given below are correct?

A
  • miR-122 stimulates HCV RNA synthesis prior to promoting viral protein synthesis by displacing PCBP2 from the viral RNA genome via competition with PCBP2 for binding to the 5’ UTR. This mode of action promotes an open, noncircular genome conformation
33
Q

What are the mechanistic features of the miR-122 function during HCV replication? Which statements are correct?
- The cellular miR-122 binds to the 3’ UTR and to the 5’ UTR of the viral genome.
- The binding sites for the cellular miR-122 are exclusively located in the 5’ UTR of the viral genome.
- The mode of action of the cellular miR-122 on HCV replication mainly based on the inhibition of translation of the viral RNA by binding to the 3’ UTR of the viral RNA.
- The mode of action of the cellular miR-122 on HCV replication is mainly based on the increase of stability of the viral RNA by binding to the 3’ UTR of the viral RNA.
- The mode of action of the cellular miR-122 on HCV replication is mainly based on the increase of stability of the viral RNA by binding to the 5’ UTR of the viral RNA.
- The mode of action of the cellular miR-122 on HCV replication is only based on the negative regulation of translation of cellular liver-specific mRNAs by binding to their 3’ UTRs.

A
  • The cellular miR-122 binds to the 3’ UTR and to the 5’ UTR of the viral genome.
  • The mode of action of the cellular miR-122 on HCV replication is mainly based on the increase of stability of the viral RNA by binding to the 5’ UTR of the viral RNA.
34
Q

How are retroviruses traveling directly from cell to cell? Describe briefly the mechanism and the functional role of the cell associated retroviral ENV protein in this process?

A

ENV: promotes export of mRNA out of the nucleus

spread cell-to-cell by induction of multimolecular complexes termed virological synapses that assemble at the interface between infected and receptor-expressing target cells.

35
Q

At which membrane does the budding of retroviruses occur?
- ER membrane
- intermediate compartment
- Golgi membrane
- plasma membrane

A
  • plasma membrane
36
Q

Täterin (CD317) exerts an antiviral role. Against which virus family does it act and what is the antiviral mechanism?

A

Retroviruses (budding via ESCRT pathway) (envelope)
- Tetherin in virus membrane bins to Tetherin of CD317 in host membrane
- no budding
- vesicle isn’t released
- uptake of virus into the cell and degradation in lysosome

37
Q

Which cellular protein complexes are used by retroviruses for assembly and budding (correct full name and abbreviation).

A

ESCRT-protein complex (endosomal sorting complex required for transport)

38
Q

Viruses use cellular filopodia for cell spread. Name 3 viruses from different families and explain the mechanistic differences in their use of the filopodia for cell to cell spread.

A

a) Newly formed retroviruses accumulate on the cell surface, they surf on existing filopodia and are transported via retrograde transport on filamentous actin to the new target cell
b) long contact between target membrane and filopodia leads to their uptake, facilitates virus transmission followed by intracellular actin driven transport
c9 vaccinia virus: induces from outside the formation of actin-“comet tail”, virus is thereby transported toward target cell , actin-flow in the target cell is used for further transport processes
d) African swine fever virus, induces from inside the formation of filopodia

39
Q

The infection of members of the genus Flavivirus involves the process of membrane fusion. What is the role of prM during maturation of the visions of these viruses? Describe this process and the role of prM.

A

prM: protection form fusion during budding; Turin cleaves prM into pr and M (in TGN)

1) Co translational association with helper protein (e.g. prM in Flavi-, E2 for Alphaviruses)
2) Helper protein blocks fusion activity; protects virus from premature fusion
3) proteolytic cleavage of helper proteins is a requirement for fusion activity of the fusion protein
4) Due to a low pH in the secretory pathway, pr peptide remains bound to E even after proteolysis and still protects virus from premature fusion with the host cell membrane
5) After secretion into the extracellular milieu (neutral pH), pr peptide is released and the fusion loop in E (internal loop not terminal like class I fusion peptide) becomes fusion active
6) At neutral pH E is a dimer lying flat on the vision; at low pH in the end-some E is converted into a conformation protruding from the vision surface which allows insertion of the fusion loop onto the Endosomal membrane
7) this triggers trimerisation of E which triggers the conformational change leading to the approach of membranes and their fusion

40
Q

What is the role of prM during maturation of the virions of these viruses? Describe this process and the role of prM.

A
  • protection from fusion during budding; Turin cleaves prM into pr and M (in TGN)
41
Q

What is the role of the prM in the maturation of virions of the genus Flavivirus? Explain the fate and function of prM during virion morphogensis

A

prM has to protect E from premature fusion during assembly and budding process

prMis cleaved by Furin in the TGN into pr and M; pr remains bound to E due to the low pH in the TG and the secretory pathway and shields fusion loop of E

after budding in neutral pH is released and allows the fusion loop to act in infection

42
Q

At which step does Influenza virus interfere with the RIG I signaling pathway? Which viral protein is required for interference

A

Influenza A virus nonstructural protein 1 (NS1) specifically inhibits TRIM25-mediated RIG-I CARD ubiquitination, thereby suppressing RIG-I signal transduction.

43
Q

Describe the properties of RIG I

A

-C-terminal regulatory domain
- 5’ PPP RNA (also when ss)
- short blunt ds region (also without 5’ PPP) e.g. panhandle of ss (-) RNA virus
- poly Uridine stretches

44
Q

Describe the properties of RIG-I

A
  • retinoid acid inducible gene I
  • Helikase -> intracellular receptor
  • restriction factor
  • recognizes RNA viruses like Hepatitis C, Influenza
  • pattern recognition receptor
  • Regulatory domain
  • Helicase domain
  • cascade activation and recruitment domain
45
Q

Viruses take active counter measures against the interferon induction via the RIG-I pathway. Give one example of a (+)-strand and one example of a (-)-strand RNA virus and explain which viral proteins are used to antagonize their recognition by this pathway. Name the viral antagonists and their mode of action.

A
  • Influenza A (-ssRNA) NS1 binds TRIM25 -> no ubiquitination of RIG-1, no binding to IPS-1 -> no interferon
  • HCV NS3-4A inhibits MAVS (IPS-1)
46
Q

Link the statements (1 to 12) to the viruses (A and B) by writing the statement numbers behind the correct virus. Multiple links are possible (incorrect
answers cost points)
1. 2-,3- and S-fold symmetry
2. A hypodermic “nano”-syringe
3. Helicalsymmetry
4. 12 faces, each with a S-fold symmetry
5. 12 vertices, each with a S-fold symmetry 6. g8p major coat protein, 2700-3000 copies 7. =4
8. Amplitude and pitch
9. Jelly roll structures
10. P=µxp
1 1. Chymotrypsin-like fold 12. Canyon binder drugs
A. Phage M13: B. Picornaviruses:

A

PHAGE M13
- P = µ x p
- helical symmetry
- g8p major coat protein, 2700 - 3000 copies

PICORNAVIRUSES
- Jelly roll structures

47
Q

Assign a correct term to the numbers depicted in the schematic drawing representing Hemaglutinin!

A

1 = signal peptide
2 = silica acid binding
3 = clara cleavage
4 = fusion peptide
5 = 6-helix bundle
6 = membrane anchor

48
Q

Different statements regarding:
- Tat, transactivator of transcription
- lntegrase
- REV, regulator of expression of virion proteins
- Vif, viral infectivity factor
- Vpu, viral protein out Vpr, viral protein rapid
- Nef, non-evident function Proteinase
- Reverse transcriptase
- GP41
- GP1 20
- CA, capsid protein

A
  • Vif- viral infectivity factor: Hijacks the cellular Cullin5 E3 ubiquitin ligase to ubiquitinylate APOBEC3G
  • REV, regulator of expression of vision proteins: lnvolved in splicing and nuclear export of viralmRNA
  • RNA-RNA duplex dependent RNase activity
  • Tat, transactivator of transcription: Activates CDKg by binding to Cyclin T1 of elonqation factor P-TEFb
  • Vpu, viral protein out: lnduces ubiquitinylation and deqradation of CD4
  • CA, capsid protein: Penta- and hexamer tyPe Protomers
  • Vpr, viral protein rapid: G2 cell cycle arrest to endorse viral LTR activity
  • RNA-dependent RNA polymerase: Reverse transcriptase
  • Nef, non evident function: MHC-class-1 and -2 antiqen reduction
49
Q

Statements about GP120, Reverse Transcriptase, Vif protein, Rev protein

A

GP120: CD4 receptor binding to evoke receptor ubiquitination and degradation

Reverse Transcriptase: RNAseH Domain, tRNA(Lys3)

Vif protein: Ubiquitin ligase recruitment to degrade cellular cytidine deaminase

Rev protein: Crm1 - Ran.GTP - eIF-5A export pathway, Regulator of viral RNA splicing

50
Q
  1. Tat (transactivator of transcription)
  2. Rev (regulator of expression of Virion proteins)
  3. Vif (viral infectivity factor)
  4. Vpr (viral protein rapid)
  5. Vpu (viral protein out)
  6. Nef (negative factor/ non evident function)
    A. Hijacks the cellular Cullin5E3 ubiquitin ligase in order to label APOBEC3G for degradation
    B. is produced in an early stage of infection and plays a decisive role in the onset of events
    C. Binds to the cytoplasmic domain of the CD4 receptor and induces ubiquitinylation and degradation of the CD4 receptor
    D. Can act directly as a toxin inducing cell death via apoptosis in uninfected “bystander” T cells
    E. Promotes the RanGTP dependent export of mRNA out of the nucleus
    F. Induces the arrest of proliferating infected cells at the G2/M phase of the cell cycle
A
  1. Tat (transactivator of transcription) : D. Can act directly as a toxin inducing cell death via apoptosis in uninfected “bystander” T cells
  2. Rev (regulator of expression of Virion proteins): E. Promotes the RanGTP dependent export of mRNA out of the nucleus
  3. Vif (viral infectivity factor): A. Hijacks the cellular Cullin5E3 ubiquitin ligase in order to label APOBEC3G for degradation
  4. Vpr (viral protein rapid): F. Induces the arrest of proliferating infected cells at the G2/M phase of the cell cycle
  5. Vpu (viral protein out): C. Binds to the cytoplasmic domain of the CD4 receptor and induces ubiquitinylation and degradation of the CD4 receptor
  6. Nef (negative factor/ non evident function): B. is produced in an early stage of infection and plays a decisive role in the onset of events
51
Q

(+)-strand RNA viruses restructure the intracellular membrane systems of the host cell for their genome replication.
Name for each of the compartments listed below one virus which makes use of these membranes for genome replication:
- ER
- Golgi
- Lysosomen
- Mitochondrien

A

ER: Kunjin virus (Flavivirus)
Golgi: Kunjin virus (Flavivirus)
Lysosomen: Rubella virus
Mitochondrien: Flock house virus

ER: HCV
Golgi: Kunjivirus
Lysosomen: Rubella/Alphavirus
Mitochondrien: Flock house virus

52
Q

Influenza A virus can block the induction of interferon alpha/beta with one of its gene products. Explain based on a scheme the underlying molecuar mechanism (which viral gene product, which celular signaling molecule, how is the signaling chain interrupted).

A

Influenza A virus nonstructural protein (NS1) sepcifically inhibits TRIM25-mediated RIG-I CARD ubiquitination, thereby suppressing RIG-I signal transduction.

53
Q

Viruses use cellular filopodia for cell spread. Name 3 viruses from different families and explain the mechanistic differences in their use of the filopodia for cell to cell spread.

A

a) Newly formed retroviruses accumulate on the cell surface, they surf on existing filopodia and are transported via retrograde transport on filamentous actin to the new target cell
b) long contact between target membrane and filopodia leads to their uptake, facilitates virus transmission followed by intracellular actin driven transport
c9 vaccinia virus: induces from outside the formation of actin-“comet tail”, virus is thereby transported toward target cell , actin-flow in the target cell is used for further transport processes
d) African swine fever virus, induces from inside the formation of filopodia

54
Q

Before “p” can start the cDNA synthesis on the viral RNA an activation step is required. Describe this activation step and explain the priming reaction in detail. Name the involved molecules and explain the individual steps with a scheme.

A

All DNA-polymerases need a “primer” (3’-OH end) for initiation of DNA synthesis
- 5’ base of (-)-DNA covalently bound to tyrosine in TP-domain of P > “protein priming”
- P protein accepts no other template RNA than pgRNA (<>cDNA synthesis!=
- 5’ end of (-)-DNA localizes in 3’ proximal DR1 (direct repeat 1)
- UUC sequence in DR1 exists also in the epsilon bulge region (sequence of duck HBV)
- Its complementary sequence AAG in the (-)-DNA represents a copy thereof
- epsilon contains origin of replication for (-) DNA
- (-) DNA Synthesis is discontinuous
-> Retroviruses are similar in their mechanisms

55
Q

Describe the pathway used by SV40 to its site of genome replication

A
  1. Endocytosis into Calveolae
  2. Fusion with Caveosome, no pH shift
  3. Long transport in vesicles; actin, Rho-GTPase and microtubule-dependent into the ER
  4. Structural rearrangement of the capsid in the reducing milieu of the ER, mysristylated N-term of VP2 exposed
  5. Penetration into cytoplasm; ERAD pathway! (ER-associated protein degradation complex)
  6. Import into nucleus by NPC and NLS in VP2/3

Cell Biology (19 decks)

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