Final group of questions

Via an interrupted mating experiment 

Hfr + F- cell (with several mutations)

The Hfr and F- cells are mixed together and then samples are remvoed from the culture at various times and plated on different agar dishes lacking a variety of things

it showed that all genes being transferred are not at once, but rather occur at different times.

It is not completely accurate and is unable to distinguish the relative positions of two genes less than two minutes apart

it is not active in all mammalian cells. It is functinal in the early embryo, but after birth, it is only active in stem cells. 

it means that they shorten at every division

after 50 rounds or so of division, the cells enter a senescent state in whcih they remain alive but cannot divide. 

It is a protective mechanism that counters the tendency fo a cell lineage to accumulate defects such as broken or rearranged chromosomes. It prevents cells from becoming cancerous by ensuring that the lineage is terminated before the danger point is reached

False: Not all display senescence

Cancerous cells divide continuously in culture, their immortality being looked on as analogous to tumor growth. They may activate telomerase

Observation: It is not clear whether telomerase activation is a cause or an effect of cancer, although the former seems more ikely because dyskeratosis congenita results from a mutation in the gene specifying the RNA component of human telomerase

There are little to no therapeutic relevancies with this

Currently, the protein component is used to make vacines. And, the RNA component is thought to be able to inhibit the telomerase enzyme if it is complementary

DNA replication by regulating events at the replication origin

At the G1 to S phase transition: it can affect both the G1/S-Cdk, which will in turn affect the S-Cdk since it will not be able to accumulate and allow transition

S phase, which may cause a shunt of the pathway into apoptosis, slowing down, or stopping.

M-phase: affects the M-CDK, which allows the G2 phase transition to M phase

located in metaphase chromosome

• CENP-A makes chromosome more rigid
• CENP-A also forms the platform for kinetochore assembly

a set of genes and other DNA sequences that enable plasmids to capture genes from phages and other plasmids

icosahedral: individual protein subunits (protomers( arranged in 20 faced geometric structure that surrounds nucleic acid

filamentous: protomers arranged in helix

head-and-tail: combine both features

lytic infection cycle

take over the host cell's machinery in a way that the lytic bacteriophage takes over a host bacterium

• a) stored in the host cell prior to release, forming a crystalline inclusion inside the cell
• b) continually extruded from the infected cell; the virus particles become coated with a small part of the outer cell membrane as they are released from the cell

a type of viral retroelement encapsidted genome is made of DNA

retroviruses that cause cell transformation because of abnormalities int heir genome structures; they carry cellular genes that they have captured from previous cells they have infected

if a cellular gene replaces part of the retroviral gene complement, the virus can't replicate and produce new viruses, as it has lost genes coding for vital replication enzymes and/or capsid proteins

These defective retroviruses are not always inactive as they make use of proteins provided by other retroviruses in the same cell

retroviral: not only is it an outside thing, but it gets immediately converted into DNA and then dsDNA--> reintegratin

retrotransposition: RNA--> dsDNA--> reintegration; it is also endogenous

an active or inactive retroviral genome integrated into a host chromosome