Chapter 18 Smartwork (Exam 4) Part 2

Growth factors promote

protein synthesis and inhibit protein degradation

Death receptors are NOT

extracellular signals, they are cell-surface receptors

Some extracellular signals signals stimulate cell death by

apoptosis, but wont engage G1/S-Cdk activity

Survival factors primarily

suppress cell death by apoptosis

Which extracellular signal proteins trigger a wave of G1/S-Cdk activity?

mitogens

Mitogens stimulate the synthesis of

G₁ cyclins and G₁/S cyclins; a buildup of these cyclins triggers a wave of G₁/S-Cdk activity and entry into S phase

Alterations of p53 and Rb will

promote entry into S phase

Alterations of Cdc6 and G1-Cdk will

prevent entry into S phase

M-Cdk is activated by the removal of

inhibitory phosphate groups on it, not by phosphorylation of M cyclin

The concentration of M cyclin increases gradually throughout

G2

Why does the activation of M-Cdk begin abruptly?

each M-Cdk complex can activate more M-Cdk

The abrupt activation of M-Cdk depends on the removal of

inhibitory phosphates by Cdc25

Activated M-Cdk activates more Cdc25 and promotes

activation of additional M-Cdk through a positive feedback loop

Actin and myosin divide a cell in two during

cytokinesis

Condensins assemble along the sister chromatids at the start of

M phase and help them coil up into a more compact form

The shortening and thickening of chromosomes in M phase depends on

condensins

What does the phosphorylation of Cdc25 by M-Cdk do?

it activates Cdc25 which in turn activates more M-Cdk

The phosphorylation of condensins by M-Cdk triggers

their assembly onto DNA, compressing chromosomes into a more compact form

Why does the nuclear envelope break down at the start of prometaphase?

proteins that form the nuclear pores and nuclear lamina become phosphorylated

Nuclear lamins and nuclear pore components are

phosphorylated by M-Cdk

Kinetochore proteins assemble at

the centromere of each condensed chromosome

Microtubules capture chromosomes by binding specifically to

kinetochores on the sister chromatids

The anaphase-promoting complex or cyclosome (APC/C) triggers the onset of anaphase by triggering

the destruction of the cohesins that hold the sister chromatids together

The reassembly of the nuclear envelope at telophase depends on

the dephosphorylation of nuclear lamins and nuclear pore proteins

One approach to killing cancer cells is to

induce apoptosis

What are reasonable approaches that researchers can take to induce apoptosis in cancer cells?

• activating the Bax protein

• inhibiting Bcl2 protein

Apoptosis is mediated by a

proteolytic caspase cascade, and caspase activation is regulated by Bcl2 family ofpr oteins

Bax and Bak

stimulate apoptosis

Bcl2

inhibits apoptosis

Inhibiting G1-Cdk will prevent

entry into S phase but will not kill cells

Many cells die by

apoptosis in many normal, adult human tissues

Apoptosis occurs in

embryonic and adult animal tissues

In apoptosis, the cell undergoes an

orderly cell death right where it stands and its remains are rapidly removed by macrophages

Apoptosis depends on a

tightly regulated proteolytic cascade (caspases)

Some death-inhibiting members of the Bcl2 family inhibit apoptosis by

blocking cytochrome c release from mitochondria

Bcl2 inhibits apoptosis by

preventing Bax and Bak from releasing cytochrome c

Bax and Bak are death-promoting members of the Bcl2 family o proteins that

induce the release of cytochrome c from mitochondria into the cytosol

Cytochrome c promotes the assembly of

an apoptosome, triggering the caspase cascade

Bcl2 inhibits

apoptosis THUS it cannot be considered to be death-promoting

Apoptotic cells

shrink and condense

• die neatly without damaging their neighbors

Cells that die by necrosis

swell and burst, spilling contents over their neighbors

What structural changes are typically seen in a cell that undergoes apoptosis?

• the cytoskeleton collapses

• the cell develops irregular bulges

• the nuclear envelope disassembles

Bax and Bak trigger the release of

cytochrome c and promote apoptosis

Mutations that prevent Bcl2 family proteins Bax and Bak from interacting with the outer mitochondrial membrane would have what effect?

preventing the release of cytochrome c and inhibiting apoptosis

Bak and Bax promotes cell death by

triggering the release of cytochrome c into the cytosol

The origin recognition complex (ORC) binds to

replication origins throughout the cell cycle

In G1 phase, ORC associates with the

G1-specific protein Cdc6 to recruit helicases to the prereplicative complex

How does S-Cdk prevent re-replication?

phosphorylation of ORC and Cdc6

S-Cdk prevents re-replication of the genome by

phosphorylating the ORC and Cdc6 complexes

Separase is the enzyme that cleaves

cohesin molecules

The protein securin holds separase in

an inactive form until anaphase onset, when securin is cleaved by APC/C complex

Cohesin is cleaved by the enzyme

separase which is held in an inactive state by securin until its degraded by the APC/C complex