BCMB30002: Functional Genomics & Bioinformatics Question Thread

[MelonBar]

Hey guys, I thought I'd start up this thread because there's a few of us taking the subject, though I'll probably be asking all the questions!

My first question is about ChiP-Seq, specifically about the figure A in the pic I'm posting from a review article (freely available from the Cell website so I presume I can post it). Btw its also on slide 6 of lecture 2 from marie and the full article is the first link on google when you type in the title "transcription factors: specific DNA binding and specific gene regulation" by Todeschini, Georges, Veitia.

I get the red dots are TFs binding to different DNA molecules, but I don't really get where the DNA molecules are from, and how they can be aligned like this. are the DNA molecules from the same genome? If they are, on what basis can you actually align them like that so as to get the high, med, low occupancies. If there are different regions in the genome where the TF binds, why can you align them this way. I just don't get anything about this...

[vox nihili]

Pretty sure they sequence a few genomes at once, rather than just look at the one. Then the number of red dots is the number of times they find that TF bound to that particular sequence of DNA. TFs that are always bound (under particular conditions) will have a higher number of reads and thus more occupancy.

[MelonBar]

Thanks t rav. also, do you have any idea whats going on in slide 12 of silkes 1st lecture? Ive wasted so much time trying to understand whats hes saying. has the human cell been genetically engineered to express the yeast UAS?

Also is the whole point of the slide just to demonstrate the concepts in signalling? Such a complicated way to do things...

[vox nihili]

Thanks t rav. also, do you have any idea whats going on in slide 12 of silkes 1st lecture? Ive wasted so much time trying to understand whats hes saying. has the human cell been genetically engineered to express the yeast UAS?

Also is the whole point of the slide just to demonstrate the concepts in signalling? Such a complicated way to do things...

yeah pretty sure it has been engineered. Think that slide was more of a "look how cool the shit I do is" kind of thing than something we actually need to know (I hope)

[MelonBar]

Haha yeah hopefully, but its hard to gauge what you need to know for john's section. Eg, at the end of john's 3rd lecture, he goes on for a while about the molecular switch of MLKL... and I think hes drawing stuff on the board which isnt captured. SO ive been trying to look up the primary source but I dont understand anything lol.

And the slides not in the lecture file. So hopefully that was just extra

[vox nihili]

Haha yeah hopefully, but its hard to gauge what you need to know for john's section. Eg, at the end of john's 3rd lecture, he goes on for a while about the molecular switch of MLKL... and I think hes drawing stuff on the board which isnt captured. SO ive been trying to look up the primary source but I dont understand anything lol.

And the slides not in the lecture file. So hopefully that was just extra

I know exactly what you mean there. I'm a little worried about his stuff too. In his tute he did tend to focus on the bigger picture though and didn't seem too bothered by details, so I think I'll probably just focus on the broader details myself (partly because I haven't even started revising yet)

[MelonBar]

PSA: assignment marks are out

[heart]

at last got 25/30 passing should be a bit easier now lol

[vox nihili]

Mine aren't yet 

[mahler004]

Mine aren't yet 

Some of the lecturers took a little longer irrc. Depends on the topic you did.

[vox nihili]

Some of the lecturers took a little longer irrc. Depends on the topic you did.

Yeah three of them finished weeks ago but the fourth hadn't yet. They were waiting to release them all together I think

[MelonBar]

Am I the only one freaking out?

Btw, any predictions for John's section? I feel like he asked the main question in MST2, about apoptosis/necroptosis with diagrams. But he's going to have three questions. Any ideas? I honestly don't know what else he can ask really.

Also, a question about apoptosis. When the NFkB pathway is interfered with by the pathogen etc cFlip stops being transcribed, activating caspase 8 which cleaves RIP1. This then leads to apoptosis - do we need to know more than this?

And, the bax/bak apoptosis happens by a different mechanism in development etc right? It doesn't have to do with the TNF signalling ? Are you guys learning about the non-TNF apoptosis? The stuff with the cytochrome c leaving the mitochondria etc. I don't think he was too clear in his explanations for this.

Thanks!




















This is easily the hardest subject I've taken at uni and I'm on the verge of giving up. ammmm i actually going crazy?

[MelonBar]

Hope you guys did alright today. Wasn't john's Q5 pretty much identical to his SAQ in MST#2?

Thank fuck there was no question on splicing

[ChickenCh0wM1en]

Hope you guys did alright today. Wasn't john's Q5 pretty much identical to his SAQ in MST#2?

Thank fuck there was no question on splicing

How'd you go? I heard it was pretty darn hard :O

[vox nihili]

Hope you guys did alright today. Wasn't john's Q5 pretty much identical to his SAQ in MST#2?

Thank fuck there was no question on splicing

I give this 6 and 2/3 an upvote



You're not wrong about John's. Except that it was shorter than his SAQ thank God. Only asking about cell death rather than anything else.

Thought Ian's question about specific gene translocations was a bit rough. Perhaps I missed it, but I can't remember him really speaking about anything other than the Philadelphia chromosome.