Can you help with my science question? – Friday 13th Nov

So today was a little of a disaster if I’m honest. I arrived at 8:30am to find out the mutants I thought I’d made yesterday weren’t real 😦 . They didn’t grow on my antibiotic plates overnight. This means I’ll have to try again next week. On top of that I managed to get dangerously close to my bunsen burner and nearly set my hair on fire (I didn’t, but it was close). I have an ear infection so wasn’t feeling great, luckily one of the post-docs kindly agreed to supervise my undergrad in the lab so I could work on the computer instead, and not risk any more bunsen related mishaps.

I worked away at the computer this morning, aiming for inbox zero, I managed to achieve inbox 1 so I’m quite happy with that. I also did some reading and researching. If anyone knows anything about homologous recombination and the possibility of it occurring independently of recA or a site specific recombinase please, please, please get it touch. I need to know.

Ok desperate plea for help over :P. Due to the previously mentioned ear infection I left work at 1pm today as I had a doctors appointment. This meant I missed the weekly team meeting, but I did put together some slides anyway. I handed them over to the boss & went through them with him, so he can give a quick update on my work. We also spent 20mins going through what I’d found out and what I was planning to do next week. The only question I wasn’t able to answer was the homologous recombination one above. Seriously need to work that one out! Seriously.

So only a half day to tell you about today. Hopefully by Monday I’ll be fully recovered and back to lab work. So until then, have a great weekend everyone, and thanks for reading.

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4 thoughts on “Can you help with my science question? – Friday 13th Nov

    • Hi thanks for getting back to me! 🙂
      I work on a system that’s phase variable via DNA inversions on several pairs of inverted repeats. The system contains it’s own tyrosine recombinase, but loss of the recombinase doesn’t eliminate all inversions, only inversions on the smallest of the repeats. This suggests to me that inversions on the smallest repeat are done by site specific recombination using the recombinase but there must be an additional mechanism to facilitate DNA inversions. Knocking out RecA doesn’t prevent DNA inversions and I’ve been systematically making single and double knock outs of all the recombinases in the genome (bacterial) that I’m able to, without any success in preventing inversions. My current working hypothesis is that the size of the inverted repeats (>300bp for one of them) allows for recombination without any kind of intervention but I’m hoping to find something in the literature that backs up that this can happen at the rate I’m seeing, otherwise I might need to start making triple mutants! :O
      Any help would be fantastic 🙂

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  1. Sounds like a fascinating puzzle, but phase variation unfortunately, is not an area i’m all that familiar with. I think your explanation makes sense and i hope you figure it out. Keep blogging your progress, id love to see how this plays out. Sorry for my lack of help on this one.

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