Voice 260530_132738
Mga Kabanata
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0:00Kabanata 1: I have the same things in my mind. 299s · Speaker 1
I have the same things in my mind. I just looked very clear into it yesterday. How was the practice yesterday? I know it's short, like five minutes. It was good. Any comments or any subjections? Yes, I discussed with Dr. Thay. T -E -H, Dr. …
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5:00
you know how to do it and we are going to expand the gene pool and look at more genes because we don't think those are the candidates and then next is that how we gonna I don't want to say many because it's difficult so the next things that…
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7:35Kabanata 3: Oh, okay. 66s · Speaker 1
Oh, okay. And then maybe, let's say, I guess it would be 2 ,000 or something, 1 ,500. I don't know, but maybe I'm not. I don't know. It's just my thinking. Okay. So, I think that I'm thinking now. So, for example, I just checked yesterday. …
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8:42Kabanata 4: Really? Are you sure? 299s · Speaker 6
Really? Are you sure? Yes. That's so little. That's so few. Or... Okay. Okay, okay, okay. The filter that I use is to... yeah because yeah because 4 ,000 gene and then yeah high -impact SNP and then SV okay I will give you the exact number …
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13:43
The structure is a very small survey, like just the length. Maybe we can add with the Hayten data, this one, like the structure of synaptomal complex. So then we can conclude that Hayten is less and structure... Okay, because you mentioned …
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18:46Kabanata 6: They are not. 300s · Speaker 1
They are not. They don't, I mean, I don't think they... So maybe these... You know what I mean? So SPOI -11 is expressed everywhere and then they bite to the chromatin but only the chromatin SPOI -11 association attack it on the axis. It's …
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23:46Kabanata 7: Because ATACs require a lot of fresh cells. 297s · Speaker 1
Because ATACs require a lot of fresh cells. So that's difficult. I already published data, maybe. I will send you a link. Okay. So maybe we will use that. Otherwise, we will not do. Yeah, we don't propose something we cannot do. So the DNA …
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28:48Kabanata 8: But we have only few name lines which have, we didn't have I think all the. 301s · Speaker 2
But we have only few name lines which have, we didn't have I think all the... Right, so we, we, we, we, I mean, our lab check 10, I think, was K10. Okay. And for those 10, so for those 10 name lines, we check K10. And all these seem to do a…
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33:50Kabanata 9: if they are 16 so all other 15 lines has different polymorphism Only this is specific, exclusively, only present in 72. 278s · Speaker 1
if they are 16 so all other 15 lines has different polymorphism Only this is specific, exclusively, only present in 72. We pick up this. And it is not necessary that this will always reduce the growth rate. Maybe it can increase the growth …
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41:07
But because these are just 98, so I'm thinking maybe if we... But now, because now you are filtering out from 26, 25 plus B73, right? Because we don't know, we should only look at... the line that has been studied for a crossover and then w…
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46:07Kabanata 11: mentioned some genes like the crossover 2 and ZIP1 expression is high at the zygoteen stage, which is critical for ZIP1. 300s · Speaker 1
mentioned some genes like the crossover 2 and ZIP1 expression is high at the zygoteen stage, which is critical for ZIP1. So that expression of ZIP1 is high in Zygoteen. So that's voice file to check. So maybe ZIP1 is forced to... Right. So …
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51:08Kabanata 12: I can use any file. 64s · Speaker 1
I can use any file. I see. And if my screen is on, it's just... I know. You can see the mouse is... Yeah, moving. So that's why I just... Off my... Off, yeah. Okay. All right, all right. So, uh... Why I did not satisfy with my progress? Nev…