Cell Energetics

 Energy and Metabolism (8)

 Cellular respiration (9)

 Some basic questions:

1. How do enzymes work?
2. Why do we have a body temperature?
3. What happens to the food we eat?
4. Why do we need oxygen to breathe?
What is energy?
 The ability to do work.
What is biological work?
 Muscular contraction> “active” transport
 Conducting nerve impulses> “active” transport
Energy has different forms
(Ex: Heat [random motion of molecules], Light, Chemical, Mechanical, Nuclear)
Has two states
Potential Energy- stored energy
Kinetic Energy- energy created from movement
Thermodynamics- study of energy
 1st Law: Energy transformed, not created or destroyed
 2nd Law: Energy transformations aren’t 100% efficient
-Lose energy as heat
Cells
 Many reactions need energy input to go
-Called “Activation energy”
 How can organisms overcome this?
-By influencing chemical bonds
-Done with enzymes (catalysts)
-Make reactions “go faster”
-How? “Changing the shape” of molecules
Endergonic: “opposite”
Exergonic: products have more free energy than the reactants/ “Energy releasing”

Enzymes
 Form temporary association with substrate(the substance the enzyme works on)
 Enzyme remains unchanged
-can be used again
 Unique 3-D shape
-Have areas on surface where substrate binds
*Called “active” sites- substrate fits with enzyme
Lock and Key Model
Enzyme>key (stays the same)
Lock>lock (changes)
 Enzymes are usually proteins
Ribozymes – RNA acting like an enzyme

Enzymes
 Example: carbonic anhydrase
 Remember this?
-Takes carbon dioxide and water and creates H2CO3
 Reaction needs activation energy
-No enzymes: 200 molecules/hour
-Enzymes: 600,000 per second
Enzyme Activity
 What factors affect them?
-Concentration
*of enzyme and substrate
-Temperature
*Optimum in human body: 35-40 Celsius
-pH
*Affects H-bonding
*optimum 6-8
 Also affected by other chemicals
 Bind to enzyme and change its shape
-Activators: keep enzymes in configuration
-Inhibitors: decrease enzyme activity
 Competitive Inhibition: when the inhibitor and substrate compete to bind with the
active site
 Non-competitive Inhibition: when the inhibitor binds with the allosteric site to
turn the enzyme on/off
Coenzymes
 Often involved in cell energetics
 Carry electrons-involved in redox rxns
-Redox: Reduction: gain e-
Oxidation: lose e- ( Oxygen causes substances to lose electrons)
 Always coupled
-One atom reduced, other atom oxidized
 Play key role in E flow
- e- represent stored energy
- Coenzymes accept and then pass e-
NAD+: a coenzyme (first character in the play)
 NAD+ = Nicotinamide Adenine Dinucleotide
 NAD+ is oxidized form
 If it picks up 2 e- and 1 H+
-Hydrogen atom
>1 proton (H+)
>1 electron
-becomes NADH (reduced)
  2 Coenzymes
NAD+
FADH (oxidized form)
Falvin adenine dinucleotide
Chemical E in the cell: ATP
 Why are e- transferred in the cell?
-To manufacture ATP
*Adenosine triphosphate
*Structure: nucleotide-like
 Energy stored in bonds between P groups
-unstable
 Think of coiled spring
 When bonds between P broken: E release
-ATP->ADP + P (+ E released)
 Used for what: Endergonic reactions
 Energy is not stored for a long time in ATP, energy is stored in fat
 ATP unstable, so is made constantly
-Only a few seconds worth in body
-Fats: long-term E storage
 How do cells make ATP?
-Cellular respiration: Chapter 9
Metabolism- sum of all energy conversions
 **Catabolism: “breaking down” reactions**
 Anabolism: “building up” reactions
-How does catabolism happen?
-Metabolic pathways: -series of reactions in the cell
-Products become reactants in the next step
-Enzymes regulated
Aerobic Cellular Respiration reaction
Food + Oxygen -> Energy (released) + Carbon Dioxide +Water
-> ATP
Glucose + Oxide -> Carbon Dioxide + Water
C6H1206 + 6O2 -> 6CO2 + 6H2O

No Oxygen: anaerobic
Pathways of Aerobic Respiration
1. Glycolysis
2. Oxidation of Pyruvate
3. Krebs cycle
4. Election transfer chain
Glycolysis = “sugar breaking”
 Start with =glucose (1 molecule=6 carbons)
 10 step pathways
 End up with 2 three-carbon molecules = Pyruvate
 Where? In cytoplasm
  By-products? 2 net ATP(3.5% of potential energy of glucose)
Expends 2 ATP
Makes 4 total
 ATP is made by Substrate-level phosphorylation
-enzyme catalyze formation directly from an intermediate of glucose
-different than in mitochondrion
 NADH gets formed (2 molecules)
-NAD+ -> NADH by picking up e-/ H+ from glucose
Oxidation of Pyruvate – in the mitochondria
 Pyruvate is oxidized =loss of electrons
 Pyruvate (3 carbons) -> acetyl. CoA (2 carbons) +CO2
 2 NADH is formed (1 from each pyruvate)
Krebs cycle –in mitochondria
 nine reactions
 acetyl. CoA (2 carbons)
 oxaloacetate (4 carbons)
 the acetyl. CoA and the oxaloacetate combine to form citric acid (6
carbons)
 By products =Krebs
-for each acetyl. CoA -get 2 CO2
-get 1 ATP
- get 3 NADH
- get 1 FADH2

Electron Transfer Chain (the electrons are being held in the coenzymes…NADH,
FADH2)
 So what is left of glucose?
 Electrons and protons
 Where are they?
-Carried by coenzymes
-For each glucose:
*10 NADH
*2 FADH2
 Electron Transport Chain- in mitochondria across the inner membrane
 Electrons in coenzymes (NADH)
 Passed to NADH dehydrogenase (protein in inner membrane)
 Electrons picked up and passed from carrier to carrier in the membrane
 Passing of e- generates H+ (proton) gradient
 H+ build up in intermembrane space
 Where do the electrons ultimately end up? Accepted by oxygen
 Makes water in the process
 H+ in the intermembrane space flow back to the matrix through ATP synthase
(enzyme)
- mechanical energy generated
- ATP gets synthesized
 (this type of ATP formation=chemiosmosis > oxidative phosphorylation)
For each NADH > 3 ATPs
For each FADH2 > 2ATPs
From 1 glucose = Yields 36 ATP
What happens to fats/proteins?
- Broken down into amino acids
- Have to be deaminated (take the NH2 group (amino group) is removed)
-Waste is urea
Fats go through B-oxidation and end up in the Krebs cycle
-the Acetyl CoA is produced through a two carbon group and then goes to the
Krebs cycle
Anaerobic Respiration- O2 not final electron acceptance
Fermentation: product of glucose is the final e- acceptor
Two types:
1. Alcohol Fermentation: yeast
~ Goes through Glycolysis, makes two pyruvate and CO2 is released to
produce 2 Acetaldehyde is made-picks up e- and ethanol is produced
~ 2 ATP powers yeast
2. Lactic Acid Fermentation:
~ Goes through Glycolysis, makes two pyruvate which is the final e-
acceptor and the molecule of Lactic Acid is made
~ Muscle cells deprived of oxygen
Chapter 11- How Cells Divide

Zygote: when you are one cell/ when the sperm and the egg as gomates fuse together
- Egg and Sperm cells are haploid (half = each with 23 chromosomes) and
zygote (diploid: full set of chromosomes = 46 total) (One set of
Chromosomes from each parent)
Mitosis: Definition?
- Nucleus Replication (each of the 46 chromosomes are replicated exactly)
- 1882 – Fleming: coined “mitosis”- Greek for thread( threads refer to
chromomsomes)/ observed chromomsomes from salamanders
- Chromosomes = units of DNA + protein
Chromosomes structure
- Homologues: in nearly identical pairs ( has 23 sets of Homologues)
- Each has similar structure and genes
- Composition: 40% DNA, 60% protein
- The protein protects the DNA and provides structure
- Very tightly coiled ( =condensed)
- Coiling: DNA wrapped around histones
- Histones are glopular proteins the DNA wraps around
- Cluster of 8 histones for every 200 nucleotides
- This unit: a nucleosome
Chromosomes
 Condense during mitosis
 Appear in “X” shape when replicated
  Duplicated chromosomes ~ 2 sets of identical DNA after S phase
 Two equal halves are called sister chromatids
Observing Chromosomes
 Karyotype: an array of chromosomes an individual possesses
 Often done during amniocentesis
During mitosis
 Microtubules attach to chromosomes
 Eventually pulls them apart
 Attached at area called kinetochore…
 Spindle- arrangement of microtubules that will pull apart the chromosomes
 Centrioles- organelles that arrange the spindle
 The aster (means star) contains the centrioles
Mitosis
 Four phases: Know pp. 215-218
 Prophase: chromosomes condense, nuclear envelope breaks down, spindle forms
 Metaphase: chromosomes line up at metaphase plate
 Anaphase: spindle pulls the chromosomes to either pole of cell
 Telophase: chromosomes “unwind,” nuclear envelope reforms…
Cytokinesis
 Cell completes division
 Animals: cleavage furrow forms…
 Plants: cell plate forms…
Regulation of Cell Cycle
 “Checkpoints” present
 Where growth can be arrested...
 G1/S Checkpoint > is growth ok for mitosis?
 G2/M Checkpoint > are chromosomes duplicated ok?
 Spindle checkpoint > are chromosomes attached to spindle ok?
Control of cell cycle
 Checkpoints “controlled” by kinase enzymes:
 Add P to activate proteins
 Internal Regulation
 Cycle also controlled by “growth factors”
 External signals
Application: Cancer
 What is cancer? > unrestrained mitosis
 Failure to regulate cell division
Control of Cell Division
 Gene in our cells called p53
 P53 gene codes for a protein called p53
 P53 monitors integrity of DNA in G1
 Is DNA damaged or OK?
 If damaged: p53 initiates repair or apoptosis ( cell death)
 In many cancerous cells: p53 is absent
  Cigateete smoke can damage p53
Meiosis (Ch12)
 Main question: how do cells become haploid?
 Diploid (46 chr.) > haploid (23 chr.)
 Meiosis: Occurs in germ-line cells producing gametes
 Germ-line cells are cells that will start out diploid and end up haploid ( ovaries in
a female: produce eggs / testes in a male: produce sperm)
 Van Beneden-1880s Dutch scientist
 Studied Ascaris gametes
 First to say: fertilization (syngamy) of haploid gametes forms diploid zygote
Meiosis: unique features
 Synapsis: homologues pair up side by side/ held together by protein bridge/
synaptonemal complex
 Recombination: genetic exchange during synapsis/ occurs by crossing over/
chromosomes pieces switch places/ Site of crossing over: chiasma
 Reduction division: 2 rounds of cell division
The Phase of Meiosis
 Meiosis 1: first nuclear division
-P, M, A, T (1)
 Meiosis 2: second nuclear division
-P, M, A, T (2)
 Events of meiosis: know pages 234-235
Some points to remember
 Metaphase I: homologues paired up
-One goes to each new cell
-Sister chromatids not split in Anaphase I like in mitosis
 Meiosis II proceeds like mitosis
-Sister chromatids split
 Meiosis end result: 4 daughter cells, each haploid
Combination
 How many different chromosome combinations can there be in gametes?
2 to the “n” power
- n = number of homologues
- If n = 2, then 2 to the second power = 4
- If n = 23, then 2 to the 23rd = 8,388,606
Why? Homologues line up randomly at metaphase of meiosis I
 called independent assortment
Chapter 13

Guiding Questions for this Chapter

1. Why do organisms appear the way they do?
2. Why are there patterns in way traits are inherited?
3. How are traits in inherited?
Gregor Mendel
1. pea plants-model organism why peas? Accessible/ short life span/ distinct traits
(flowers: purple or white/ short or tall/ seeds: yellow or green)/ the traits were
segregated/ easily manipulated flowers and reproduction
2. investigated patterns of inheritance
3. mid 1800s
4. first to systematically record observations
5. quantified (mathematically and statistically figured out patterns) patterns of
inheritance
6. Did his work in Austria
7. Catholic monk
8. Overturned 2 big misconceptions
 species were constant (never changed)> Paradox?
 traits were directly inherited (traits blended)>
What was an example of one of Mendel’s first monohybrid experiments?
- took true-breeding purple- flowered peas
- true-breeding meaning: homozygous dominant (2 “purple” genes)
- true-breeding purple-flowered peas times true-breeding white peas = ? all offspring
purple flowers (F1 generation)
- F1 purple times F1 purple = 3 purple plants: 1 white plant (F2 generation)
- Purple = dominant
- White = recessive
- Monohybrid = examined one trait
- Dihybrid = exanime 2 traits at once
How do Mendel’s explanations match up with our modern understanding of genetics?
- Mendel predicted: traits were coded for in the organism by “factors” “genes” today
- 2 factors for every trait in each organism predicted “Meiosis”
- Factors come in different forms or versions today = alleles
What do the following terms mean: heterozygous/homozygous; genotype/phenotype;
dominance/recessiveness?
- heterozygous: 2 different alleles for a gene
- homozygous: 2 of the same alleles
- genotype: set of genes possessed by an organism
- phenotype: physical expression of these genes
- dominant: allele expressed regardless of the other allele
- recessive: allele expressed only in the presence of another one like it
How can genetic problems be solved systematically? What does a Punnett square
represent?
1. symbolize alleles (P= purple allele p = recessive white allele)
2. Genotype of parents: purple times purple (true breeding)
PP times PP
3. Punnett square- problem of fertilization
- figure out gametes
- fertilization
Mendel’s first experiment was a cross of PP times pp producing all purple or
heterozygous Pp
Second experiment was a cross of Pp times Pp producing 3 purple and 1 white
Each box has a potential genotypes for of the offspring
Outside the box are the parental gamates

Dihybrid cross (seed experiment)

R = round
r = wrinkled
Y = yellow
y = green
F1 example: RR YY (round, yellow) times rr yy (wrinkled, green) = all turned out to be
round, yellow (heterozygous)
F2 example: RrYy times RrYy
RY Ry rY ry Phenotype Ratio?
RY RRYY RRYy RrYY RrYy 9/16  round, yellow (both dominant)
Ry RRYy RRyy RrYy Rryy 3/16  round, green (one dom, one rec)
rY RrYY RrYy rrYY rrYy 3/16  wrinkled, yellow (one dom, one r)
ry RrYy Rryy rrYy rryy 1/16  wrinkled, green (both recessive)

Yes, two traits behave independently EXCEPT WHEN…they are on the same
chromosome!!!!
Why aren’t the patterns of inheritance for most traits explained by simple Mendelian
genetics? What are examples of each of the explanation?
Why aren’t most traits “Mendelian”?
- traits are usually are more complicated than Mendelian’s
Why aren’t patterns of inheritance for most traits explained by Mendelian genetics?
A. polygeny- most traits coded for by many genes (ex: human height / continous varition)
B. pleiotropy- one gene that has many different phenotypes
C. epistasis- when one gene influences expression of another
- Example: corn plants- color in kernals (Effect pigment: A and B gene both
dominant alleles needed for color)
D. environmental effects- ex. Temperature cold temp. white fur and whenever it
becomes warmer it gets darker in warmer temp.
E. incomplete dominance- in heterozygous individuals- “blending” of alleles neither is
dominant = partial expression of each
- Example: Japanese four o’clock
Cr = red
Cw = white
Cr Cw = pink
F. multiple alleles: Human blood typing – ABO system
IA = galactosamine –RBC surface marker
IB = galactose – RBC surface marker
i = no sugar expressed
IA IA= type A= IA IA IB = type AB (+)(-) = Rh factor separate marker
IB IB = type B= IB ii = type O on sep.gene
- O negative = universal donor = no antigens  (surface marker)
- AB positive= universal recipient = has all the antigens
H. Sex-linkage: gene on sex chromosomes (X or Y)
Ex: Color blindness in humans
XC = color vision / Xc = color blind
Homework example: Xc Y x XC Xc
XC Xc
X X X Xc Xc
c C c

Y XCY Xc Y 50% males

Specific gene mutation?
- cystic fibrosis: Cl ion channel
- sickle-cell anemia: disorder on red blood cells/ folded red blood cells
- Hemoglobin defective
- recessive- 2 copies of the bad gene for disease
- high resistance to malaria
- Huntington’s disease: symptoms don’t show up until middle age
Chromosomal disorder?
-non-disjunction failure of chromosomes separate in meiosis
-Down syndrome: 21st
-Klinefelter: male’s XXY breast development and mental retardation
-Turner: female’s X nothing  mental impairment and sertile
- triple X: female’s XXX
- Jacob’s: male ‘s XYY