cytoskeleton II Flashcards

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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
Q

where are lamellipodia found? how do they function?

A

Tips of growth cones; filled with actin; myosin is required for contraction of cell

26
Q

what effect does a contact-mediated attraction/repulsion cue have on growth cones?

A

contact with an adhesion protein in the substrate (use adhesion protein as traction)

27
Q

what effect does a chemoattraction/chemorepulsion cue have on growth cones?

A

attraction to an emitted chemical cue

28
Q

what does embryonic development depend on and why?

A

Actin and tubulin are essential for embryonic development; bc it requires extensive cell movement

29
Q

what can a mutation on PIP5KI gene cause? what is it associated with? what can it lead to?

A

myocardial developmental defects; associated with impaired intracellular junctions; lead to heart failure and extensive prenatal lethality at embryonic day 11.5 of development

30
Q

why does the mutation in PIP5KI happen?

A

Actin disorganized and cadherin missing (calcium dependent adhesion protein)

31
Q

what other aspect depends on cell migration and adhesion? what condition can it cause if done incorrectly?

A

neural tube closure; spina bifida

32
Q

what are sertoli cells? what role do they play in kennedy disease? what are the symptoms of the disease?

A

respond to androgen and make sperm; alterations in the sertoli cell cytoskeleton during development produce infertility and facial/throat muscle weakness

33
Q

how are sertoli cells modified to cause the disease?

A

have altered cytoskeleton and lack androgen receptors on nucleus

34
Q
A