Cell and molec Exam 2

Function of Electron transport

Break the large free energy drop from food to oxygen in a series of smaller steps that release energy in manageable amounts

Chemiosmosis

Coupling of the redox reactions of the electron transport chain to ATP synthesis

Cellular Respiration Overall process

Organic compounds + O2 -> CO2 + H2O + Energy

C6H12O6 + 6O2 -> 6CO2 + 6H2O + Energy (ATP + heat)
(sugar)

phosphorylation

Transfer of the terminal phosphate group from ATP to another molecule

Alternatives to ATP

1-GTP
2-Creatine phosphate

Anabolic Processes

Build Molecules, increase order, and require energy (sun energy)

Catabolic pathways

Break down molecules, reduce order, and hydrolyzes sugar

Energy enters the system as

Light

Redox Reactions

Release energy when electrons move closer to electronegative atoms

Oxidation

Loss of electrons

Reduction

Gain of Electrons

In cellular respiration, Glucose is _____ and O2 is _____

Glucose - Oxidized

O2 - Reduced

cellular respiration uses an electron transport chain to break the fall of electrons to O2 into several steps.

electron transport chain

Electron transport chain

Consisting of several molecules (primarily proteins), is built into the inner membrane of a mitochondrion.

NADH shuttles electrons from food to the “top” of the chain.

At the “bottom,” oxygen captures the electrons and H+ to form water.

Electrons are passed by increasingly electronegative molecules in the chain until they are caught by oxygen, the most electronegative.

ATP synthase location

Mitochondria and Chloroplasts

Glycolysis Net results

2 ATP (from 4)
2 NADH
2 Pyruvates

In the energy payoff phase, ATP is produced by

Substrate-level phosphorylation

Fermentation

Pyruvate ---> Lactate using a NADH

What are some substitutions for glucose?

Lactose, Maltose, and Sucrose

Starch

Glucose storage molecule

Krebs cycle and Electron transport occur in

Cytoplasm of Mitochondria

ATP synthase pumps a ATP per

3 Protons pumped

Summary of TCA cycle

Net yield is 4CO2, 6NADH, 2FADH2 and 2 ATP for each glucose molecule

Two carbons make 4 Acetyl CoAs

Oxidation occurs at 4 steps with NAD+ as the electron acceptor in 3 cases (producing 3 NADH) and FAD as the electron acceptor in one case producing FADH2

ATP is generated at one point with a GTP intermediate by substrate level phosphorylation

Only a fraction of 38 ATP ultimately produced by respiration of glucose are derived from substrate-level phosphorylation.

4 or 4/38

ATP synthase

In the cristae uses the energy of the proton gradient (between intermembrane space and Mitochondrial Matrix) produced by the electron transport chain to power ATP synthesis.

Mesophyll layers

Filled with chloroplasts

Chloroplasts

Light harvesting system of the plant

Stoma

Turgor pressure and CO2 control

Light dependent reactions

Light excites electrons driving ATP production in ETC
4 Protons for 1 ATP

Stroma ----> Intermembrane space gradient

Light independent reaction

Calvin cycle - produces triose phosphate

Light strikes pigment - electrons passed to another until central chlorophyll a molecule

What helps with other pigments that chlorophyll doesnt cover?

carotenoids and phycocyanin

Light harvesting pigment

Hydrocarbon tail that interacts with hydrophobic neighbors
Central Magnesium that carries electrons
Porphyrin Ring

How does the light harvesting pigment work

When light strikes electrons jump to a higher energy level then donate to an electron acceptor. Then they are carried on magnesium

Noncyclic Electron flow

-Light excites electrons that are passed to p680
p680 gives electrons to primary Acceptor

-Oxygen evolving complex splits H2O molecules

PSII

25 polypeptides where two bind chlorophyll P680 and components of the ETC system.
Four manganese atoms aid in the oxidation of water

Cytochrome b6 complex

Seven polypeptides and includes two cytochromes and iron-sulfur

PSI

10 Polypeptides and binds chlorophyll P700 and Several additional electron carriers

How does a hot day affect stoma?

Hot day =

Stomata closes (increases water, limits photosynthesis)
⬆️O2 ↓CO2

These conditions favor Photorespiration

Why is photorespiration an evolutionary relic?

Because Rubisco first evolved at a time when the atmosphere had far less O2 and more CO2

C4 plants

Mesophyll and Sheath Cells

CAM plants

Open stomata at night (DAY) CO2 ---> Organic Acid ---> CO2 -----> Calvin cycle

Hatch-Slack cycle (C4)

Malate formation - Burns ATP

- Incorporates CO2 in four-Carbon compounds (oxaloacetate)

Calvin cycle three phases:

–Carbon fixation (catalyzed by rubisco)
–Reduction
–Regeneration of the CO2 acceptor (RuBP)

Apoptosis

Cell and organelles shrink and shrivel, membrane stays intact

Doesnt induce inflammation

What are the two ways apoptosis is activated

Cell-surface death receptor - Extrinsic

Mitochondrial membrane - Intrinsic (Bcl2)

Cytochrome C

Leads to Activation of programmed cell death

Bcl2

Family that regulates intrinsic pathways

Necrotic Cell death

Leaks cell contents and induced inflammation

Phagocytes role in apoptosis

Swallowing apoptotic cells before they do damage

Eicosanoids

Mediate inflammatory responses

CycloOxygenases

Turn FFAs into prostaglandins and eicosanoids

Facilitates inflammatory responses

Aspirin (Cox1 and Cox2)

CycloOxygenase (inflammation) inhibitors

Necrosis leads to

Vasoconstriction
⬆️Blood flow
⬆️Tissue temp and Reddening
⬆️Capillary permeability (White blood Cells)

What is pus

Dying white blood cells

Caspase Enzymes

Proteases that drive apoptosis by inactivating apoptosis inhibitors

How do caspases work

Initiator caspases signal other caspases to induce apoptosis

Effector caspase cleaves proteolytic targets

Cellular proteolysis targets

-Nuclear
-DNA Related
-Cytoskeleton
-Cytoplasm
-Protein Kinases

What are some roles of Apoptosis?

-Sculpting tissue (shaping fingers)
-Deleting structure
-Removal of unwanted cells
-Forms Amniotic Cavity

Apoptosis pathway

Initiator caspase --> Effector Caspase ---> Apoptosis substrates

Intrinsic pathway

-P53 activation
-Controls p53 target genes initiating cell cycle
-Cells release BH3 if cell cycle isn't initiated
-Cytochrome C releases from mitochondrial pore
-Caspase 9 activation ---> Caspase 3/7 ----> 8

Extrinsic pathway

-Ligand binds to death receptor
-Recruits FADD protein
-Caspase initiation (Caspase 8)
-Cleaves caspase (3 & 7)
-Apoptotic substrates activated

Heptameric apoptosome

7 Apaf-1 units with associated cytochrome C molecules

Inhibitors of Apoptosis proteins

Final line of defense against apoptosis, bind to caspases

P53

Upregulated by DNA damage

Induces death genes like BH3

Causes cell cycle arrest

Activates BAX proteins to trigger activation of caspase-9

MDM2

Regulates P53 by INHIBITING IT

Phosphorylated (inhibited) by ATM / ATR when cells are damaged

AKT

Activates MDM2 to regulate P53 by inhibiting it. Promotes cell growth, proliferation, and survival, targeting P53 for degradation.

DNA Damage Path

DNA Damage ➡️ ATM/ATR activation ➡️ Inhibition of MDM2 + Activation of P53 ➡️ Cell Cycle Arrest or Apoptosis

Typical signal transduction pathway

-Membrane receptor responds to ligand
-Receptor phosphorylation starting activity
-Recruits adapter / scaffolding proteins
-Adapter protein phosphorylated
-Transcription factor activated
-Activate gene expression through promoter

Hormone pathway

Hormone ---> Bloodstream ---> Diffuse into cell ---> hormone receptor ----> Promoter attachment

Local signaling

Animal cells may communicate by direct contact

Gap Junctions - Animals
Plasmodesmata - Plants

Local messengers - Short distance messengers (ex. Secretory vesicle / neuron)

Endocrine gland

Produces hormone and releases adjacent to bloodstream into vessel to target cells

Hormones

Lipid soluble and bind to receptors inside cell to trigger changes

Saltatory conduction

Jumps from nodes of Ranvier to another

Myelin sheath

Protects axon and facilitates signal

MS & CIDP

Degenerated myelin sheath which leads to slower conduction of signals

The three Cell signaling stages

Reception - Receptor in plasma membrane binds to signal molecule (conformational change)

Transduction - Relay molecules in signal transduction pathway

Response - Change in gene expression (activation of enzymes)

Three main types of membrane receptors

• G-protein linked receptors
  - Receptor tyrosine Kinases
  - Ion channel Receptors

G-protein linked receptor

Plasma membrane receptor with a heterotrimeric G protein (ex. RAS). Bound to G protein = Inactive, switches GDP to GTP.

Examples of G proteins

Olfactory receptors
Thyroid stimulating hormone receptor
Opioid receptors

Receptor tyrosine Kinases

Membrane receptors that attach phosphates to tyrosines. Recruit relay proteins that lead to different cell responses.

Ion channel Receptor

Gate when receptor changes shape. Allows specific ions in.

2nd Messengers

Small, nonprotein, water-soluble molecules / ions. Can spread through diffusion. Initiated through G-protein (ex. cAMP, Ca2+, IP3, DAG).

Adenylyl Cyclase

Enzyme in the plasma membrane that turns ATP into cAMP in response to a signal

Phosphodiesterase

cAMP ----> AMP

Regular G-protein pathway with cAMP

First Messenger ---> G-protein linked receptor ----> G protein ---> Adenylyl cyclase ----> (ATP --> cAMP) ----> Protein Kinase A ----> Cell response

cAMP response element (CRE)

Area on promoter where activated PKA can bind to boost transcription

CREB

Crucial cellular transcription factor—a protein that binds to specific DNA sequences (CREs) to regulate transcription of target genes.

CRAC (Calcium Release-Activated Calcium)

Specialized calcium ion channels in the plasma membrane that open to allow extracellular calcium into the cell via Store-Operated Calcium Entry (SOCE).

Calmodulin

Wraps around proteins inducing conformational changes when calcium is added