Evolution Lecture 15

Front 1

H1N2

Back 1

Surface proteins on influenza; Hemagglutinin / Neuraminidase

Front 2

Brevig18

Back 2

Spanish influenza; all influenza can be traced back to this one

Front 3

Over time, influenza diverges genetically...

Back 3

at a linear rate. It also experiences antigenic drift.

Front 4

What do we need to figure out in order to create designer vaccines?

Back 4

Patterns of substitution: These help us 'predict' next year's virus.

Front 5

Patterns of subsitution

Back 5

Most amino acid substitutions occur under Positive Darwinian Selection

Front 6

Jaeken Syndrom Symptoms

Back 6

Developmentally disabled; skeletal deformities; abnormal distribution of fat; impaired liver function

Front 7

Jaeken Syndrom Cause

Back 7

Autosomal Recessive; 24 lof mutations in PMM2 on Chromosome 16

Front 8

Senescence

Back 8

Aging

Front 9

Heritability of Life Span

Back 9

0.17 to 0.35 in homo sapiens

0.34 in caenorhabditis elegans (worms)

Front 10

Antagonistic Pleiotrophy in terms of longevity

Back 10

One gene controls more than one trait; one is beneficial (early in life) and the other is deleterious (later in life)

Front 11

Within vertebrates, bats and birds...

Back 11

Have metabolic rates and absolute sizes that are inconsistent with other vertebrates; perhaps flying keeps you safer/alive longer

Front 12

Animals on islands tend to be _________ lived

Back 12

Longer-lived; fewer large predators

Front 13

p53

Back 13

Cancer suppression

Front 14

Four Models of Aging

Back 14

-Rate of Living Hypothesis

-Mutation Accumulation Hypothesis

-Antagonistic Pleiotrophy Hypothesis

-Disposable Soma Hypothesis

Front 15

Rate of Living Hypothesis

Back 15

Postulates that the faster an organism's metabolism, the shorter its lifespan. The theory was originally created by Max Rubner in 1908 after his observation that larger animals outlived smaller ones, and that the larger animals had slower metabolisms.

Front 16

Mutation Accumulation Hypothesis

Back 16

Suggests that the evolutionary effect of adverse events declines following the age at which an organism is initially capable of reproduction... aging is caused by random mutations causing adverse aging characteristics.

Front 17

Antagonistic Pleiotrophy Hypothesis

Back 17

A gene controls more than one trait; one is beneficial (early in life) and the other is deleterious (later in life) and causes either aging or death

Front 18

Disposable Soma Hypothesis

Back 18

Presumes that the body must budget the amount of energy available to it. ... It is the compromise in allocating energy to the repair function that causes the body gradually to deteriorate with age VS reproduction.

Front 19

Apert Syndrom Symptoms

Back 19

Retruded midface, fused fingers and toes, prematurely fused cranial sutures, heart defects, etc // bones fuse too early in development

Front 20

Apert Syndrom Cause

Back 20

Autosomal dominant; mostly spontaneous mutations; germline sperm cells with this mutation are faster BUT have phenotypes that reduce adult fitness

Front 21

Testis Age; Paternal Age Effect

Back 21

Younger men have more neutral mutations; as the man gets older, selfish mutations with deleterious variants become more common; eventually the man becomes sterile