Ahmad Lectures

Question 0

Emx2

Answer 0

Open-lip Schizencephaly (cleft-lined with gray matter, connecting subarachnoid space with the ventricular system)

Question 1

Otx2

Answer 1

Mutation causes microophthalmia or aniridia

Question 2

Wnt

Answer 2

Presence of Wnt allow for target genes to be activated and B-catenine to be produced

Question 3

Wnt1 & FGF8

Answer 3

Secreted by the isthmus and cause activation of engrailed (En) transciption factors

Question 4

Engrailed Genes

Answer 4

Activated via Wnt1 and FGF8; cause differentitation of mid brain stem cells

Question 5

Hox Genes

Answer 5

1. Are regulated by concentration of retinoic acid (increases concentration in posterior end
2. They regulate the motor neuron identity in the hindbrain

Question 6

SHH (sonic hedgehog) Genes

Answer 6

1. SHH (released from the notochord and floor plate) binds to Patched (PTC) which causes it to be inhibited so Smoothened (SMO) can activate Gli to activate gene expression
2. Mainly turns stem cells of the ventral surface into motor neurons

Question 7

BMP

Answer 7

1. Released by surface ectoderm and the roof plate

2. Turns stem cells of the dorsal surface into sensory neurons

Question 8

RA/FGF Factors

Answer 8

Required to help motor and interneuron differentiation

Question 9

Chordin/Nogin

Answer 9

Needed to suppress the dorsalizing effects of BMP in the ventral part of the neural tube

Question 10

Notch Receptor

Answer 10

Causes Gene Repression - heterodimeric receptor in the plasma membrane (are 4 types; Neurogenesis uses Notch 1)

Question 11

Delta & Serrate (Jagged)

Answer 11

Ligands that bind to the Notch receptor, causes the cells to remain uncommitted due to inhibition of proneural genes

Question 12

Proneural Genes

Answer 12

1. Helps the cell differentiate into a different cell

2. Inhibited by Notch receptor binding to Delta and Serrate (Jagged)

Question 13

Retinal Ganglion Cells

Answer 13

Take visual field information out of the eye to the brain

Question 14

PDGF

Answer 14

1. Platelet derived growth factor produce in utero that differentiates Type 1 Astrocytes into O2A Progenitor cells
2. Cells lose the response to PDGF after birth

Question 15

CNTF

Answer 15

1. Produced by Type 1 Astrocytes after birth, help differentiate O2A progenitor cells into Type 2 Astrocytes with the help of ECM factors from mesodermal cells
2. Also can be used to rescue neurons from death/is an important neurotrphic factor

Question 16

Oligodendrocyte Development

Answer 16

Type 1 Astrocyte > PDGF > O2A Progenitor > No CNFT > Oligodendrocytes

Question 17

Type 2 Astrocyte Development

Answer 17

Type 1 Astrocyte > PDGF > O2A Progenitor > CNTF & ECM factor > Type 2 Astrocyte

Question 18

Filopodia

Answer 18

Slender motile extensions that sample the environment and then either extend or retract

Question 19

Lamellipodia

Answer 19

Spaces between the filopodia

Question 20

Laminin

Answer 20

Major component of the basal lamina and are responsible for the growth promoting ability of the ECM…will bind to integrin

Question 21

Integrin

Answer 21

Are receptors on growth cones that will bind to laminin and cause cytoskeletal rearrangement that propel the filopodia

Question 22

Cadherin

Answer 22

1. A group of cell adhesion molecules that promote calcium dependent cell adhesion
2. Mediates stronger cell adhesion needed for tissue histogenesis and integrity…without it, fetuses will die

Question 23

Catenin

Answer 23

Link cadherin molecules to the cytoplasm

Question 24

IgG-Like Adhesion molecules

Answer 24

1. A group of cell adhesion molecules that promote calcium independent cell adhesion. 2. Important in fine tuning the adhesion and growth processes...loss is a mild phenotype

Question 25

Slit Genes

Answer 25

Expressed on midline cells in the brain and repel any axons possessing the Robo receptor

Question 26

Robo (roundabout) Receptors

Answer 26

Axons with these receptors will not be able to cross the midline because they are repelling by the Slit ligands on the midline cells

Question 27

Robo3

Answer 27

Anti-Robo that down-regulates Robo1/Robo2 which allows an axon to cross midline

Question 28

Netrin

Answer 28

1. A glycoprotein that is drawn to a DCC receptor and attracts axons from dorsally located commissural neurons toward the midline in the floor plate 2. Also can mediate repulsion if DCC and UNC-5 receptors are expressed at the same time on the same axon

Question 29

UNC-6

Answer 29

1. A homologous gene to Netrin in c. elegans | 2. A mutation in this gene causes uncoordination because it prevents axons from reaching and/or crossing midline

Question 30

Semaphorin

Answer 30

Are secreted (long-range) and membrane bound (short-range) ligands that cause the collapse of growth cones

Question 31

Ephrin A

Answer 31

Membrane-bound ligand tethered to glycosyl-phosphatidyl-inositol (GPI) and interacts with EphA causing a repulsion

Question 32

Ephrine B

Answer 32

Transmembrane ligand that interacts with EphB causing a repulsion

Question 33

Eph Receptors

Answer 33

A receptors that binds Ephrin...causes a repulsion and prevents midline crossing and helps determine where in the axons of the RGC terminate in teh tectum (superior colliculus)

Question 34

NGF or trkA

Answer 34

2 nerve growth factors in the Neurotrophin class that if absent would result in the absence of sympathetic ganglia

Question 35

NT3

Answer 35

A nerve growth factor in the Neurotrophin class that if absent would result in a reduced number of sympathetic ganglia

Question 36

Bcl-2 and Bcl-xl

Answer 36

Anti-apoptotic, found in mitochondria, ER, and perinuclear membrane, will promote the survival of sympathetic neurons in the absence of NGF and inhibit Bas and Bad

Question 37

Bax and Bad

Answer 37

1. Pro-apoptotic factors, induced by withdrawal of NGF of injury 2. Will cause the release of cytochromme C which will then go on to activate caspase 9

Question 38

DP5/Hrk

Answer 38

1. Induced by NGF-deprivation, oxidative stress, or an increase in calcium 2. Helps activate Bas by translocating Bas from the cytosol into the mitochondria where it can cause the release of cytochrome C which will activate caspase 9

Question 39

Cytochrome C

Answer 39

A soluble electron transport protein (a strong pro-apototic signal) that activates caspase 9 leading to PCD

Question 40

Par4

Answer 40

1. An essential pro-apoptotic element in the developmental and pathological neural death, particularly in Alzheimer's disease 2. Activated by oxidative stress and an increase in calcium conceentration and induces mitochondrial dysfunction by inhibiting Bcl-2

Question 41

Apaf2

Answer 41

1. Helps to transmit apoptotic signals (cytochrome C) from the dysfunctional mitochondria to activate caspases 2. Forms a complex with cytochrome C and active Caspase 9 (this is an energy dependent step that requires ATP)

Question 42

Caspases

Answer 42

1. Cysteine proteases that activate each other in a cascade in response to apoptotic signals 2. They cause DNA damage by activating DNase and by cleaving poly-ADP-ribose-polymerase (PARP), a DNA repair enzyme

Question 43

IAPs

Answer 43

Critical regulator of PCD as they influence both extrinsic and intrinsic PCD pathways by inhibiting caspases

Question 44

X-IPA & Survivin

Answer 44

Best known IAPs

Question 45

Mn-SOD

Answer 45

1. A key anti-oxidant enzyme that protects cells from apoptosis by inhibiting the formation of reactive oxygen species (= oxidative stress) 2. Oxidative stress activates DP5/Hrk and Par4

Question 46

Telomerase

Answer 46

1. An enzyme that adds 6-base DNA sequences to the ends of the chromosomes, preventing their shortening and protecting them during chromosomal segregation in mitotic cells (increased resistance of neurons to apoptosis)

Question 47

NF-kB

Answer 47

1. A transcriptional factor that if we lost, would cause neuronal cell death 2. Plays an important role in suppressing PCD by up-regulating the expression of anti-apoptotic proteins, Bcl-2, IAPs and Mn-SOD

Question 48

Phases of PCD:

Answer 48

1. Survival Phase 2. Initiation Phase 3. Effector Phase 4. Degradation Phase