cytoskeleton II Flashcards

1
Q

what forms microtubules? how is it done?

A

subunits of tubulin; Alpha and beta tubulin subunits bind GTP; alpha keeps it in structure, beta can use it

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2
Q

how does growth occur in microtubule formation?

A

at beta end of tubule

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3
Q

how do microtubules demonstrate dynamic instability? what does it mean?

A

= either catastrophe or rescue; sudden conversion from growth to shrinkage and vice versa

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4
Q

what is catastrophe? rescue?

A

catastrophe = growth to shrinkage
rescue = shrinkage to growth

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5
Q

where does nucleation occur in microtubule formation? what does this? is there a specific quantity that needs to be made?

A

Nucleation occurs in the MTOC (centrosome) using gamma tubulin and other proteins that serve as a “template” for the 13 protofilament structure

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6
Q

what is the centrosome and what does it include? how does it relate to microtubule formation? when else is it important?

A

Centrosome is a microtubule organizing center (MTOC) with embedded centrioles and nucleation sites: important during mitosis; microtubules grow from here

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7
Q

what is the function of kinetochore, non-kinetochore, and astral microtubules?

A

kinetochore = hold onto chromatin and centrosome
non-kinetochore = push/pull to separate cell
astral = anchor spindle poles to cell membrane

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8
Q

what are cilia and flagella made of? what produces their movement?

A

Made from microtubules and motor proteins; axoneme

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9
Q

what function does a flagella give a cell? what about cilia?

A

allows it to swim through liquid media (propels cell); beat rhythmically and move fluid over cell surfaces

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10
Q

what is the difference bw cilia and flagella?

A

cilia are shorter, do not move cells

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11
Q

what are 3 examples where cilia is found?

A

respiratory tract, gut epithelium, inner ear hair cells

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12
Q

what is an axoneme? what is it made of?

A

core of cilium/flagellum; Made of microtubules and associated proteins in a special pattern

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13
Q

Explain how bending works within microtubules.

A

Linker proteins stop microtubules from sliding, make them bend instead

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14
Q

what is a disorder caused by hereditary dynein deficits? what does the disorder entail?

A

Kartagener syndrome; chronic lung disease due to insufficient movement of cilia; also embryonic development issues

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15
Q

what causes Kartagener syndrome?

A

mutations on two genes on chromosome 9 cause defect in dynein arms; this leads to paralyzed cilia which causes syndrome

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16
Q

what is primary cilia? what is its purpose? where can it be found?

A

nonmotile cilia that all cells have; Act as responder to external environment, serves as signaler or receptor (antennae); nasal epithelial cells

17
Q

where are intermediate filaments found? some examples of these filaments?

A

Found in vertebrate cells that are required to deal with mechanical stress (nuclear, epithelial, axonal)

18
Q

what characteristics about intermediate filaments makes it different from the other proteins?

A

do not contain a nucleotide binding site (not ATPases), not polar (both ends of the proteins are the same), not clear how they assemble

19
Q

what is the most diverse family of intermediate filaments? what do they do?

A

Keratins; These anchor to desmosomes or hemidesmosomes

20
Q

what happens to defective keratin?

A

Alterations in keratins lead to unusual “blistering” diseases, it no longer holds the cell in place

21
Q

what’s an example of a condition caused by keratin defects? what does it cause?

A

epidermolysis bullosa; skin ruptures or blisters with any mechanical stress

22
Q

where are neurofilaments important? where are they found and how do they contribute?

A

important in axons, esp. during development; these contribute to axonal diameter which is then important for speed of action potential

23
Q

what can alteration and accumulation of neurofilaments cause?

A

ALS- muscle atrophy and filament breakdown

24
Q

what is the function of growth cones? why do they do this?

A

find and form connections with other cells; grow or shrink based on environmental cues

25
where are lamellipodia found? how do they function?
Tips of growth cones; filled with actin; myosin is required for contraction of cell
26
what effect does a contact-mediated attraction/repulsion cue have on growth cones?
contact with an adhesion protein in the substrate (use adhesion protein as traction)
27
what effect does a chemoattraction/chemorepulsion cue have on growth cones?
attraction to an emitted chemical cue
28
what does embryonic development depend on and why?
Actin and tubulin are essential for embryonic development; bc it requires extensive cell movement
29
what can a mutation on PIP5KI gene cause? what is it associated with? what can it lead to?
myocardial developmental defects; associated with impaired intracellular junctions; lead to heart failure and extensive prenatal lethality at embryonic day 11.5 of development
30
why does the mutation in PIP5KI happen?
Actin disorganized and cadherin missing (calcium dependent adhesion protein)
31
what other aspect depends on cell migration and adhesion? what condition can it cause if done incorrectly?
neural tube closure; spina bifida
32
what are sertoli cells? what role do they play in kennedy disease? what are the symptoms of the disease?
respond to androgen and make sperm; alterations in the sertoli cell cytoskeleton during development produce infertility and facial/throat muscle weakness
33
how are sertoli cells modified to cause the disease?
have altered cytoskeleton and lack androgen receptors on nucleus
34