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MTC > MTC Exam III part III > Flashcards

MTC Exam III part III Flashcards

1
Q

microfilaments

A

actin polymers. help form microvilli. involved in cell shape, contraction, and intracellular trafficking

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2
Q

microtubules

A

made of tubulin and microtubule associated proteins. extend the length of the cell. important for mitotic spindle, cilia, flagella. major system of intracellular trafficking

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3
Q

What kind of change is likely to lyse a RBC?

A

a dramatic change in surface area

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4
Q

describe the “fishing net structure” of an RBC

A

short activin filaments and spectrin molecs are located below the plasma membrane
specrin is composed of triple alpha helical and beta subunits which associate in an antiparallel manner
they attach to ankynin complex, which attaches to band three (tm bicarb transporter)
spectrin als attaches to band 4.1R, which attaches to glycophorin C

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5
Q

describe vertical interactions in rbc structure

A

spectrin/ankynin/band 3 interactions; spectrin/actin/band 4.1R GPC interactions

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6
Q

hereditary spherocytes

A

cell shabe disorder with problems with vertical interactios of RBCs.
leads to spherical RBCs
autosomal dominant most of the time
less surface area
cells ge trapped in spleen
leads to hemolytic anemia, jaundice, and splenomegaly.
treatment: spleen removal (but probs with infection and iron/folate deficiency)

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7
Q

heterotypic vs. homotypic CAMs

cis vs. trans interactions

A

CAMs: integral membrane proteins that help cells adhere to each other
homotypic bind cells of same cell type; heterotypic bind cells of different cell types
cis binds cells on the same plane of the cell membrane; trans on different planes

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8
Q

4 types of junctions

A 
anchoring junctions (structural integrity of tissues)
occluding (prevent traffic thru intercellular space)
channel-forming (enhance chemical and electrical coupling of cells)
signal relaying: enhance cell-cell communication
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9
Q

classes of CAMs

A

cadherins, IG superfamily, integrins, selectins

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10
Q

cadherins. structure and types

A

E, N, and P. single pass TM. N terminal is extracellular, C terminal interacts with actin cytskeletion via alpha or beta catenin. require Ca2+

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11
Q

pemphigus vulgaris

A

autoimmune skin blistering from desmosomal cadherins
autoimmune response against desmoglein.
flaccid blisters

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12
Q

bullous pemphigoid

A

auto antibidies agasint hemidesmosomes which attach cells to the basal lamina
deeper, tensor leisons than pemphigus vulgaris

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13
Q

cell-matrix adhesion: outside in mechanism

A

ECM ligand biding causes integrin clustering. the active receptor conformation is straight out rather than folded. active form causes binding to a linker protein to the cytoskeleton

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14
Q

muscular dystrophy

A

DGC complex normally spans the muscle cell membrane and connects actin to the cell membrane. dystrogylcan and other protiens for the DGC complex. mutations in the DMD gene on X chromsome lead to less dystrophin which leads to weakness and muscle wasting. death and neuropsyche complications possible

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15
Q

convergent extension

A

change in cell packaging leads to movement

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16
Q

ameboid migration steps

A

extension, adhesion, translocation

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17
Q

describe how actin works wrt ameboid migration. include the proteins (2) that are critical for this process

A

globular actin is activated by ATP in nucleation process to form protofilaments
protofilaments bind to form d helical filaments
new actin is added to the plus side
ATP binds to the mins side
Arp2/3 complex and formins attach actin filaments to each other
Arp2/3 links the negative ends to the middle of other actin filaments to form a branched array
formins nucleate straight, unbranched filaments to each other.

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18
Q

ameboid extension

include the protein family and activation details

A

actin polymerization pushes a part of cell forward
rearrachement of the actin cytoskeleton under the control of Rho family monomeric GTPases. GTPases normally inactive but are activated by membrane bound guanine nucleotide exchange factors (GEFs). once activated, they help control Arp2/3 and formins

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19
Q

what proteins mediate the translocation step of ameboid migration?

A

myosin motors

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20
Q

Kti/Steel: what is this? for what cells is it important? what might we see in a heterozygote?

A

example of a survival factor/receptor pair needed for cell migration. found in germ cells, blood cells, neural crest cells. receptor is kit, survival factor is steel. kit heterozygotes have piedbaldism and possible mast cell leukemia, germ cell and GI tumors

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21
Q

describe the notch receptor structure and synthesis

A

single pass receptor. extracellular domains have lots of EGF-like repeats. synthesized in the golgi as a single peptide. then cleaved such that receptors are heterodimeric.

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22
Q

notch signaling pathway: what is the ligand? what happens upon binding?

A

DSL ligands found on nearby cells
when ligand binds, notch receptor undergoes two more cleavages. this releases an intracellular tail that goes toth the nucleus to bind a TF called CSL, which is a transcriptional activator (without tail, CSL actively inhibits notch targets)

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23
Q

alagille syndrome

A

JAG1 mutuation, which we thing is a DSL ligand
autosomal dominant
intraheptatic biliary hypoplasia leading to jaundice, cardiac probs, skeletal abnormalities/butterfly vertebrae, ocular abnormalities, facial abnormalities

24
Q

CADASIL

A

cerebral arteriopathy, autusomal dominant subcortical infarts, leukoencepalpathy. notch 3 mutation.

25
Q

TGF-beta receptors: type and structure

A

ser/thr kinases
2 types
type II homodimers bind ligands, then recruti, phosphorylate, and activate type I homodimers to for a heterotetramer

26
Q

what happens upon ligand binding to TGF-b receptors

A

type II homodimers recurit and activate type I homodimers. together, they transduce they phosphorylate a smad. this smad associates with smad4. together, the smad complex goes to the nucleus and activates target genes

27
Q

What Smads mediate TGF transcription vs BMP?

A

Smad 2 and 3 is TGF; Smad 1,5,8 is BMP

28
Q

what are the 5 levels of TGF regulation

A
  1. TGF secreted into ECM in inactive form and not activated without help of throbospondin
  2. TGF antagonists exist
  3. so do inhibitory smads (smad6 and smad 7)
  4. co-receptors
  5. receptor decoys: bind the receptor but don’t trigger the pathway
29
Q

HHT/Osler-Rendu-Weber syndrome

A

heretiary hemorrhagic telangiectasia
autosomal dominant
vascular dysplasia, lung, liver, and brain involvement with lots of bleeds
mutations in Eng, Alk1 or Smad4: probs with TGF-beta pathway

30
Q

From what to arterio/venous malformations result in HHT? (4)

A
  1. loss of a/v identity in development
  2. abnormal vascular remodeling
  3. apoptosis of capillary epithelial cells
  4. dilation of anastamsoes because of loss of vascular smoolth muscle.
31
Q

PAH: pulmonary artery hypertension

A

symptoms: SOB, increased R ventricular work and right ventricular failure
problem with TGF-B signaling with BMP, whish is neeaded for early vasculogenesis.

32
Q

Marfan syndrome

A

affects ocular (myopia, displacement fof the lense, retinal detachment, glaucoma, cataracts), skeletal (bone overgrowth and jt laxity), and CV systems (aortic dilation and rupture, mitral valve prolapse, tricuspid valve prolapse). due to FBN1 mutations. caused by lack of fibrillin, which is needed in elastic and non-elastic tissues. And, FBN1 usually helps keep TGF-beta latent: FBN1 problems lead to over expression of TGFbeta signaling and excessive bone and aortic growth

33
Q

loeys-dietz syndrome

A

similar to marfan syndrome but due to TGFbeta receptor issues (aortic aneurysi, arachnodactyly, etc.

34
Q

from what are the limbs derived?

A

lateral plate mesoderm

35
Q

Which T box genes are critical in the legs? In the arms?

A

Tbx 4 in legs and 5 in arms

36
Q

describe proximal/distal limb growth orientaiton

A

controlled by AER (apical ectodermal ridge), which produces Fgfs 2,4, and 8.
progress zone is proximal to AER and consists of undifferentiated mesenchyme. the longer the time spent in the zone, the more distal the bone. Fgf4 expression maintained by Shh from the ZPA

37
Q

describe dorsal/ventral specification of limb

A

dorsal identity determined by Wnt signalling pathway. Wnt indirect induces dorsal identity. ventral identity is the default (En1 signaling)

38
Q

anterior/posterior specification in limb

A

anterior: thumb; posterior: pinky
controlled by zone of polarizing activity (ZPA) in the posterior region. ZPA confers posterior identity to limb cells using a Shh gradient
ZPA specified by Hoxb8 gene and regulated by retinoic acid. Shh expression maintained by Fgf4 form AER and vice versa.

39
Q

Holt-Oram

A

TBX5 gene mutation leading to upper limb defects and congenital heart problems

40
Q

GLI-3 defects

A

lead to brain and hand malformations

41
Q

forebrain brain development: what determines anterior/posterior patterning?

A

Goosecoid from prechordal plate

42
Q

brain devo: what determines dorsal/ventral patterning in the brain?

A

two opposing gradients: ventrally, it is Shh expression; dorsally, it is BMPs
together make a differential gradient

43
Q

holoprosencephaly definition

A

single cerebral ventricle

44
Q

SHH structure and synthesis

A

must be activated by an auto cleavage process. N-terminal signal seq is cleaved. the remaining peptide is cleaved into 2 halves by addition of acholesterol moiety to the C terminal of the half that was original the N terminal.

45
Q

SHH signaling

A

SHH activated (requires cholestero). Shh goes to surface receptor PATCHED (aka PTCH) PATCHED releases Smo, which carries out a signaling cascade in the cell

46
Q

general structure of a motile cilia

A

microtubule based organelle: 9+2 configuration

have hyneine and radial spokes

47
Q

structure of a non-motile cilia

A

9+0 config with no dynein arms

48
Q

What organelles are necessary for ciliogenesis? Where do they come from

A

basal bodies. can either come from mitosis or from generative complex/deuterosome

49
Q

What two proteins are important for intraflagellar transport system?

A

kinesin2 brings molecules to the cilia tip and dyneine2 brings stuff back

50
Q

how do motile cilia work?

A

sliding of the doublets against each other
there is an A and B tubule in each doublet. dyneine arms extend form A towards B (inner and outer), and radial spokes connected dynein arms around the central microbutule. sliding of doubles in a ATP dependent fashion occurs

51
Q

Primary Cilia dyskinesia

A

autosomal recessive disorder characterized by chronic upper resp. infection and situs inversus

52
Q

nodal vesicular parcel model vs. 2 cilia model

A

two models to explain how cilia are important in left/right determination
NVP: vesicles filled with Shh and retinoic acid are screted on the right side of the nod and are swept to the left via cilia. vesicles then open and cilia on the left of the node are chemical sensors
2 cilia model: motile cilia create a leftward flow sensed by left immotile cilia. cilia are mechanical sensors in this model.

53
Q

what two senses require cilia?

A

smell and sight (rods and cones)

54
Q

Bardet-Biedl syndrome

A

obesity, retinal rod/cone dystrophy, polydactyly, cog impairment, hypogonadism, UG malformation and nephropathy
genes are involved in IFT, esp. in parts of the brain that control hunger

55
Q

Polycystic kidney diseases

A

autosomal dominant involving kidneys, liver, pancreas

primary cilia defects:

56
Q

pallister-hall syndrome

A

autosomal dominant
hypothalamic probs, epiglottis, laryngeal cleft, pulmonary segmentation, polydacly
caused by GLI-3 problems. GLI3 mediates SHH pathway thru distal IFT
without SHH, GLIR represses SHH genes (retrograde transport of GLIR to cell body). with SHH, SMO is releases and transported to the tip such that GLIA predominates.

MTC (11 decks)

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