Any body know the answer to this?

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A bacterium harboring a 15,000-base pair (bp) plasmid that encodes resistance to tetracycline and ampicillin segregates mutants that lose resistance to either drug. Each independent mutant plasmid appears to increase in size by approximately 5200 bp. Which molecular event best explains these findings?

A ) Formation of plasmid concatemers

B ) Formation of pyrimidine dimers

C ) Homologous recombination

D ) Insertion of a transposon

E ) Slip-stranded DNA replication errors

Originally Posted by Uncle Izzy

A bacterium harboring a 15,000-base pair (bp) plasmid that encodes resistance to tetracycline and ampicillin segregates mutants that lose resistance to either drug. Each independent mutant plasmid appears to increase in size by approximately 5200 bp. Which molecular event best explains these findings?

A ) Formation of plasmid concatemers

B ) Formation of pyrimidine dimers

C ) Homologous recombination

D ) Insertion of a transposon

E ) Slip-stranded DNA replication errors

First guess would be D. I don't quite understand A, but C seems like it should lead to no size change, B and E seem like there would be a loss of size. D would lead to an increase in size. Do you have the answer?

Originally Posted by AlternateSome1

First guess would be D. I don't quite understand A, but C seems like it should lead to no size change, B and E seem like there would be a loss of size. D would lead to an increase in size. Do you have the answer?

I dont have the answer. "Just between us girls," this is a question from one of the NBME self assesments that I prob shouldnt be posting (copyright?). Then again, if they were actually giving me my money's worth, they would give me the answers and help me learn something, not just tell me what I suck at.

If anybody else out there thinks they know, that would be great.

Hey, this is way later than your post, but I think the answer is D too. Only a transposon would always cause a 5,000 bp insertion, and it sounds like the transposon is inserting and knocking out activity of either the amp or tetracycline genes

Originally Posted by Uncle Izzy

A bacterium harboring a 15,000-base pair (bp) plasmid that encodes resistance to tetracycline and ampicillin segregates mutants that lose resistance to either drug. Each independent mutant plasmid appears to increase in size by approximately 5200 bp. Which molecular event best explains these findings?

A ) Formation of plasmid concatemers

B ) Formation of pyrimidine dimers

C ) Homologous recombination

D ) Insertion of a transposon

E ) Slip-stranded DNA replication errors

I meant a transposon would cause an insertion of the same length each time

Originally Posted by marcusab

Hey, this is way later than your post, but I think the answer is D too. Only a transposon would always cause a 5,000 bp insertion, and it sounds like the transposon is inserting and knocking out activity of either the amp or tetracycline genes

Has to be D. The key is that it happens to all independently of each other, eliminating a random event or sequence.

OK - they show coagulation necrosis from an MI and ask: which of the following macrophage products is responsible for the changes seen:
a) fibroblast growth factor
b) formylated peptides
c) interfernon gamma
d) Leukotriene D4
e) neutral proteases
f) nitric oxide


Anyone know?

nitric oxide is a macrophage product that can cause cellular apoptosis. i would have thought proteases originally, but I would think that it needs to be an apoptotic thing-y. Not sure though, thats a tough question.

The picture in question sort of looked like a field of collagen and ECM that had been laid down after the MI. I put fibroblast growth factor since the fibroblasts reconstitute the ECM after the other cells die off. But I had not considered the apoptosis angle...very interesting..are people in agreement that it is nitric oxide?

Well, i think if you already at the collagen deposition stage, then FGF may be the way to go. But for pure coag necrosis and cell death (pre fibrosis-stage), Id look elsewhere.

Hey guys,

after taking the Step I today, I can tell you that the STYLE of the last question about macrophage factors is VERY HEAVILY REPRESENTED, at least on my exam. They were big on which cells release which factors

Good point about timeline of the MI!

Originally Posted by GreenT

Good point about timeline of the MI!

I agree. Coag necrosis is due to an ischemia event which usually occurs before the presence of the macrophages. Macrophages replace neutrophils approximately 5 days after MI. One of the cytokines that macrophages secrete is FGF. It activates fibroblasts to undergo the fibrosis. I would go with A.

Originally Posted by marcusab

OK - they show coagulation necrosis from an MI and ask: which of the following macrophage products is responsible for the changes seen:
a) fibroblast growth factor
b) formylated peptides
c) interfernon gamma
d) Leukotriene D4
e) neutral proteases
f) nitric oxide


Anyone know?

It's A for sure. The picture was of collagen deposition - those wavy fibers were collagen fibers FGF increases deposition of collagen and promoted Angiogenisis too.

why cant this be answer a? for the plasmid question

"

"a concatemer is long continuous*DNA*molecule that contains multiple copies of the same DNA sequences linked in series"

from <http://en.wikipedia.org/wiki/Concatemer>
..
it is made

"from result of*rolling circle replication, and may be seen in the late stage of*bacterial infection*by*phages"

from <http://en.wikipedia.org/wiki/Concatemer>

I will use this thread to put a question here. I hope someone knows. In UW they put a woman with oligomenorrhea, hirsutism and moderate obesity. Then they ask: which of the following is most likely associated? and I answered cushing syndrome. The right answer is polycystic ovarian syndrome. Why an adrenal enzyme deficienzy couldn't lead to this kind of hirsutism? Is it possible to have hirsutism + cushing syndrome?