Let me. Victoria and Pete already talk about some basics and definitions of quorum sensing so that I don't have to repeat those. So I'd like to talk about what we are doing in our laboratory in South Korea. We work on plant bacterium, which is called a gloomy. And today, I will talk about the control of primary bacterial metabolism by quorum sensing in the bulk cold area. So bulk cold area cause disease in the rice because rice particle disease and also cause bacteria wilt on many field crops, like hot pepper. And this bacterium produces the toxin, is the notorious toxin, so-called toxopulavine. It's very toxic to plant because this toxopulavine is photosensitized. So under light, they produce lots of radicals. It can be very toxic to rice. So if you go out to the rice field, you will see lots of panicle bright like this. And if you look at the individual panicles, you will see a white thing and sometimes this coloration and darkness. In paddy field, in hot pepper field, you can see a devastating wilting on the infection. So this bacteria infect roots and stems and flowers. So especially this bacterium infects rice flowers. So under favorable weather conditions, they produce lots of toxins and kills all rice panicles. Produce toxins, toxopulavine, and has only one quorum sensing system. And the optimum gross temperature is 37 degrees. And this one quorum sensing system produces two kinds of signals, one is C6 and the other one is C8. And this toxopulavine is flowering. So it's yellow color. And you can see actually the crystals of this toxopulavine on the microscope, very shiny, small crystals. So they produce lots of toxins. OK, so this is some topics we study in our laboratory using percolary glumia as a model system. We study control of primary metabolism, especially metabolic slowing and regulation of glyoxylate cycle and regulation of activated metal cycle and control of bacteria to GST. Second project is quorum sensing dependence cell death. They have very distinct cell degradation mechanism that we have not published yet. And also we study oxalazone formation and deformation, lastly, quorum sensing and genome evolution. Today I will talk about mainly the primary metabolism. For the last 15 years, we published quite a bit of papers to describe the quorum sensing system in percolary glumia. So this bacterium has one luxi and luxal quorum sensing system. It produces two signals. We don't know anything about C6-HSL, but C8-HSL is major quorum sensing signal. And top R is luxal homolog is CHHR receptor. And this tox R and C8-HSL activate another transcription activate tox J. And tox J and tox R activate tox problem biosensitizes. So that tox problem biosensitizes under control of quorum sensing. This tox top R and C8-HSL also activate QSMR. QSMR is transcription activator which belong to ICLR homolog. This QSMR activates many different kinds of genes. For example, type 2 secretion and FLHDC. FLHDC is transcriptional regulator for flagella biosensitizes and catholase genes and oxalide biosensitizes and USP genes. So this is another introduction about percolary glumia quorum sensing. Percolary glumia utilize amino acid as carbon source. So in amino acid rich medium like AB growth. So they produce a lot of ammonia because they utilize amino acid as carbon source. So in wild type, the quorum sensing system is on. So this QSMR activates OVCA and OVCB. This OVCA and OVC complex actually use acetyl-CoA and oxalate to produce oxalic acid. This oxalic acid is being secreted to the medium. So this oxalic acid react with ammonium to neutralize the environmental pH. So in wild type, this oxalic acid acts like a public good. It can be produced from QS positive strains. But in QS minus strain, there's no quorum sensing systems. So there's no oxalic acid. But they still utilize amino acid as carbon source. So they still produce lots of ammonium. So these percolary species, not only glumia, but other percolary species are very, very sensitive to high pH.  So quorum sensing mutant, if you grow them in AB growth, they die after one day because of the alkaline toxicity. So this oxalic acid is key element in percolary glumia quorum sensing systems. We have many questions, but I suggest two questions that I want to deliver today. One is individual cell to restrict neutralization on the cloudy condition as a function of cooperative activity. So on the cloudy conditions, do they really restrict nutritional acquisition? That was one question. And the other one is quorum sensing controls the primary metabolism of individual cells to maintain methoic homeostasis. So we used basically two key tools. One is transcriptome analysis. Everybody does it nowadays. And the other one is metabolomic analysis by C. top mass. C. top mass is capillary electrophoresis top mass. It's very, very different from other type of mass vector analysis. So C. top mass is very ideal mass-backed tools to analyze hydrophilic compounds. So based on our RNA-seq analysis, we found that the PTSD, which encodes phosphate protein for transfer agent, is down-regulated by quorum sensing. So we confirmed our RNA-seq data by QRT-PCR. So if you look at the wild type, this is normalized for the expression. Wild type is warm. This quorum sensing mutant is elevated. If you add the quorum sensing signal to the eye mutant, it's covered to the wild type. QSMI mutant is still a high expression of PTSD gene. This is complementation. So PTSD gene is down-regulated by quorum sensing in percolate glumine. So PTSD is very important for glucose uptake. So we did actual glucose uptake experiment using C13-labeled glucose. So we measured total C13-labeled compound by using C14-MRI. So this is the wild type, 250 micromoles. This is the quorum sensing mutant. This is complementation. And this QSMI mutant, this is complementation. So at six hours, that is just before the quorum sensing onset. So after 10 hours, concentration reaches above 10 to the 8 cells per male. So if you look at the amount of C13-labeled compound, you see more C13-labeled compound in quorum sensing mutant. This is complementation. This is QSMI mutant. So quorum sensing mutants, top five mutant and QSMI mutant, they do uptake more glucose. OK, so if they uptake more glucose, we expect they should grow much faster than the wild type. So when we monitor the growth of wild type and the quorum sensing mutant, we did see the faster growth of the quorum sensing mutant, the green and the pink. They grow much faster than the wild type. So then we were curious what happens when we culture the quorum sensing mutant and the wild type. Do they outcompete the wild type? Yes. This is the quorum sensing mutant, top R mutant now. This is the wild type. So top R mutants grow much faster and better than the wild type. So quorum sensing mutant outcompeted the wild type in the early births. So quorum sensing downregulate glucose uptake. So we wanted to conform other genes that are involved in primary metabolism by QRT-PCR. So there are a lot of genes, but this is some examples like PGK and PYK, NUOV, and this is my ATP synthase and other kinase, NDK, which is nucleoside-diposible kinase. In all cases, the origins are elevated in quorum sensing mutants. So there is a higher level of teaching expression in quorum sensing mutant. And it did complement it by adding the small quantities of signals to the mutants. So there is downregulation of whole variety of primary metabolism genes in percolate gloomy. So if there is such a wide range of downregulation of the genes that are involved in primary carbon metabolism, there should be some big changes in major metabolites in percolate gloomy. So we actually quantified some key elements by CE top mass analysis. This is some part of analysis data. If you look at the glucose 6-phosphate, for example, you see a lot more glucose 6-phosphate in quorum sensing mutant, BGS2 is top i mutant, BGS9 is QSMR mutant. So the unit is picomal potential of the nine cells. So another thing is at the ATP, if you look at the ATP levels, you see almost 3 to 5-fold increase in quorum sensing mutants. So this is a really serious problem in quorum sensing mutants. There is a huge bias in primary metabolism in quorum sensing mutants like the GTP and the PP also. So there is a huge metabolic imbalance in quorum sensing mutants. So this is negative control of primary metabolism by quorum sensing in percolate gloomy. So this is TCA cycle, and this is oxalate cycle. We call it oxalate cycle because the OVCA and the OVCB use oxalic acetate and acetyl-CoA as a substrate. It produces oxalic acid in here. Citrus synthase use same kind of substrate, but they do the conjugation reaction, the enzyme. So the blue color indicates down regulation by quorum sensing. Glucose transport and ATP synthesis oxidative phosphorylation and the PPP pentasposphate pathway and also adductor pathway. And also diatose metabolism are down regulated by quorum sensing. This is another example of down regulation by quorum sensing in gloomy. It's glutamic to uptake. So if you look at data here, this normalized C-13 labeled glutamic contents in micromole. So wild type, they uptake like 1,000 micromole after quorum sensing onset. For quorum sensing mutants, they uptake much more. So if you look at the glutamic uptake gene expression, there's a huge difference here, quorum sensing mutants. These two are complementation. So this is just another example of down regulation of primary metabolism. So if they uptake a lot of glutamate by quorum sensing mutants, there should be some problems in cellular osmolarity. So we measure the cellular osmolarity at different time intervals. After 14 hours, we see huge differences in osmolarity. These two are quorum sensing mutants. So if there is huge cellular osmolarity, something should happen to the cell. So we harvest the cells and cross section and look at the inside of cell under electron microscope. You see lots of hyperhydration here. So this is a wild type. You see intact cell envelopes. These two are quorum sensing mutants. You see lots of hyperhydration. So they do have osmolarity problem and hyperhydration phenomenon. So if we rotate GLTI, which is glutamine transporter, can we avoid the hyperhydration? Answer was yes. So this is the GLTI mutant. There's no hyperhydration. This QS minus mutant along with glutamate transporter. There's no hyperhydration. So quorum sensing mutant have several osmolarity problems. But if you knock out the glutamate transporter, you can avoid it. So glutamate uptake is really key factor to maintain cellular osmolarity. So this is a small conclusion. In part one, quorum sensing act as a metabolic break on individual cells when cells begin to mess. And quorum sensing might have evolved to ensure homeostasis of the primary metabolism of individual cells under crowded conditions. And finally, quorum sensing dependent glutamate uptake is very important to maintain cellular osmolarity in a cooperative population.  So I was talking about negative control. Now I want to talk about positive control of quorum sensing in Berkeley gloomy. So this is TCA cycle again. When I was talking about TCA cycle and people was laughing at me, it's very old classical stuff. And TCA cycle is dynamic anyway. Why do you study TCA cycle? That's true. But nobody really studied what happened to the TCA cycle in terms of population biology concept. So there is glyoxalate cycle here. And this is the oxalate cycle. The blue is negative control by quorum sensing. But glyoxalate cycle and oxalate cycle are upregulated by quorum sensing. So I'm going to talk about this. So HA is isocitrate synthase gene. And GLCP is malate synthase gene. These two enzymes are in the TCA glyoxalate cycle. So if you look at the gene level expression in the wild type, this is quorum sensing mutants, much lower than the wild type. Also GLCP, same thing here. If you add the signal to the quorum sensing mutants, it recovers or even the higher level of expression of SA and GLCP. And this is some DNA binding experiment to confirm that QSMR protein actually binds to the promoter of SA and GLCP. And this is metabolic rewiring by QS at the branch point of glyoxalate TCA cycle. So we actually measure the enzyme activity of isocitriase. And the other one is isocitrihydrogenase. So if we go back to here, this is the enzyme that are involved in isocitrate to glyoxalate. This isocitrihydrogenase convert isocitrate to alpha ketoglutarate. So here's negative control and positive control. Quorum sensing, negative control, this isocitrate dehydrate activity, I mean the transcription activity. And isocitrate liase is upregulated by quorum sensing. And also this oxalate cycle is upregulated. I didn't talk about this because it's all the stuff. So what happens when we mutate glyoxalate cycle? Why this bacter has glyoxalate cycle? Even in E. coli, we really don't know much about what the glyoxalate cycle does. What we know about glyoxalate cycle in E. coli, it is important for two carbon metabolism, like acetate metabolism. That's the only thing we know. If you look at the text book, that's the only thing you can find. And why there is glyoxalate cycle and why this glyoxalate cycle is activated by quorum sensing? That was the very, very curious question for us. So we mutated glyoxalate cycle and see what happens in terms of cooperative activity. So this is population density. This is the wild type, the blue. They grow very well. They reach over 10 cells per meal after one day. And they maintain good population density even after one week. This pink line is the OVCA mutants. This is oxalic acid minus mutant.  They collapse. This huge population collapse because they don't make oxalic acid that's probably good. The pH increase. This is the pH. If you look at the pH, which is up to 10 to the pH line. So on the high pH condition, they cannot survive. But these glyoxalate cycle mutants, they don't die. But there's this amount of decrease in population, this green line. And if you look at the pH changes, pH also increases. But not like OVCA mutant. The wild type, the pH goes up and goes down again and come back to neutralized pH. If you look at the oxalic acid production, the wild type produces lots of oxalic acid. Of course, the oxalic acid mutant do not produce anything here. Glyoxalate cycle mutant produces about 50% compared to the wild type. So what is the connection between glyoxalic cycle and oxalic biosensuses, which is the important for public good biosensuses? So first thing we did was we compared the transcriptional and translational levels of OVCA in wild type and glyoxalic cycle mutant. We didn't see much of difference of OVCA expression at transcriptional level and at translational levels. So in wild type and glyoxalic cycle mutant, OVCA was expressed at same level. Then why we don't have much of oxalic acid biosensuses in the glyoxalic cycle mutant. So this is the oxalic acid biosynthetic activity. This is actually the specific activity we measured. So after column sensing onset, the wild type shows about 40 nanomores per minute per microgram specific activity. But in the glyoxalic cycle mutant, about 20. So about 50% decrease in the glyoxalic cycle mutants. So why is that? What is the mechanism behind this data? So with these RNA signal analysis and glyoxalic cycle mutant and compared with wild type, we saw lots of differences in stress-responsive chaperone and chaperone engines like GroE-S, GroE-L, and DNAJK. OK, this is a wild type. And this is a mutant, glyoxalic cycle mutant. There is a huge difference between these two. So there was good indication that the chaperone might be involved in this business. So we wanted to confirm the RNA data by QRTPCR. This is wild type. This is a mutant. There's a huge difference here. Also, we did the Western blood analysis using anti-GroE-L. This is after 14 hours. This is wild type. This is a mutant. This is complementation. There is a huge difference even in GroE-L expression at the translational level. OK, so we observed that there is a big differences of GroE-L expression at transcription and translational levels. So what is the connection between the elevated expression of GroE-L and oxalic acid biosynthesis? So we tried many, many different possibilities. And we found out that there is a physical interruption of OVCA by GroE-L, all right? So to prove it, we did immunoprecipitation experiment. So we harvested the whole proteins and immunoprecipitated with anti-OVCA and then separated on the STSGR and the Western blood analysis using anti-GroE-L. This is the result. So this is loading control. There's an elevated amount of OVCA, GroE-L here. So if you convert this plot to the data, it's a ratio of IP readings per input readings. There is a big difference between wild type and the quorum sensing mutant. There's a more GroE-L immunoprecipitation. When we submitted this data to MBIO, the reviewers were not happy with this data. So we had to revise it and with this one more experiment. So we actually measured the OVCA activity with the BSA control. This is a non-specific protein. So we did OVCA activity experiment in vitro. And this is kind of control, a non-specific protein. So BSA added a different amount of BSA to the reaction. It did not inhibit much. But if you increase the GroE-L at a different amount, we see dramatic decrease of oxalic acid biosensitizes. So this did prove that this OVCA activity is interrupted by GroE-L. So GroE-L did inhibit the oxalic biosensitivity activity of OVCA. So if we mutate oxalic acid cycle, this bacterium experienced lots of metabolic stress. So what happened? We grew them for a longer time. Do they can survive, or do they die, or what happened to the culture? So we grew them up to seven days and take some adequate spread on the LB aga plate and observe the colony morphology. So after four days, this is the wild type, the small colony. We are seeing the big type of morphology colonies appear. So this is five days, and after six days, or seven days, almost all colonies will look like the flat and bigger compared to wild type. This is the wild type, and this is the mutant. So this is the percent of QSMR plus or QSMR minus. And if you look at the data here, this is the minus QSMR mutant. They went up to almost 90%. So we took some colonies of the big colonies and sequenced the whole genome in the beginning. And we found there is a mutation in QSMR. So this QSMR is under control of the Luxal homolog system in North Korea. Some of them had insertion in the upper reading frame. It's an IS element insertion in the beginning of the upper reading frame. And some of them had big deletion and 780 base deletion and 100 base deletions. So we found these bigger colonies have mutation in QSMR. So under metabolic stress, they have mutation in QSMR. Why? So this is QSMR spontaneous QSMR mutants. So there is an elevated activity in the QSMR mutants. Isocitrate dehydration activity increase. This is a wild type. This is the original client oxalate cycle mutants, very similar. These three are three different kinds of QSMR mutation to the client oxalate cycle. They want to mutate QSMR so that they can express more isocitrate dehydrogenase, because the client oxalate cycle is blocked. So they want to convert isocitrate to alpha ketoglutarate more under stress. So what happened to that kind of QSMR mutants? So we measure the population density at different times. So if we look at here, yellow and purple and green, they die. QSMR mutants, because they cannot activate oxalate biosynthesis. So if you look at the biosynthetic activity of oxalate here, the mutants do not make much of oxalic acid so that the pH increases. So those mutants are very similar to QSMR mutants, which cannot survive after one day. So they try to survive under metabolic stress by mutation in QSMR. But somehow they cannot survive because they cannot make oxalic acid, which is the public good. OK, so this is a conclusion based on that experiment. Quarum-sensing mediated network rewiring is very, very critical to sustain the bacterial cooperation in buccalic lumi. And we identified new roles of client oxalate cycle in bacterial population biology. And this is one good example of how molecular chaperones play important roles in bacterial cooperation. OK, so here again, to write things that we are relatively recently added to this quarum-sensing circuit in here. So this QSMR activated client oxalate cycle but repressed it because metabolism and nucleotide metabolism and also glutamate uptake. All right, so before I finish up, I'd like to thank the postdocs, Eun-hae Gu and Yong-sun Gang and former members of the students and collaborators. Sang-gi Lee is the x-ray guy who did the OVCA structural analysis. Also, Pete Grimberg who collaborated with us about buccalia malei and pseudo malei. And this is the funding agents that we got money from Korean government, the Creative Research Institute. And I will stop here, and I will be happy to answer any questions. Thank you. Thank you.


The House of Representatives considers Bill to scrap the National Youth Service Corps and Nigerians a reaction to the news. The views, if you take a look at social media, are mixed with many against the plan to scrap. The House of Representatives also fixes Jim I to begin public hearing on the review of the 1999 constitution, but we start in a series of conversations today on what women want out of the review. Today, we'll be about women participation in politics. We'll also be digging into the land grab accusation against politician Ned Moko and every other issue surrounding that accusation. Both parties at the dispute will be here this morning. Good morning and welcome to the breakfast here on PLOS TV Africa. Feels great to have you here this beautiful Tuesday morning. Thanks for joining us. I am Osaugi Ogbon. Yes, good morning. I am Annetta Felix. Good morning to you too. Morning, how are you? I'm okay. How are you? Fantastic. Ready to get straight into the business of the day. There's so much that we will be talking about. Of course, women in politics sounds pretty interesting. I would like to get straight into that and see what must change and how we should go about it. But of course, a couple of things are trending this morning. Yes, lots, lots. First of all, we're talking about the plan to scrap NYSE. So we know that there's been a lot of conversation regarding this, you know, House of Reps are always pushing for this saying we need to scrap the national youth service course scheme. And basically, you know, lots of people have been reacting to this saying, well, I don't think that should, that should be, you know, we saw a House of Reps member yesterday say that basically when youth co-members go to the place of service, you find out that employers do not, you know, want to pay them or employ them. They basically get access to cheap labor that are available. So that's that's one of the major issues here.   We've also gotten to a place where people now can lobby for where they want to be posted to so they don't go, you know, all the way to the north or the way to the south and some of all of that. And also security challenges, which I believe has to be one of the biggest, you know, reasons why there is a conversation about scrapping it, you know, because over time we've also lost dozens of core members who have gone to serve in, you know, in states far away from home and have been caught in one conflict at the other. I remember one of the elections, you know, a couple of years ago, you know, I think in 2001, I remember now, we lost, you know, about 11 or so core members to violence in the north. There's also, of course, being in the conversations concerning security with banditry now, the kidnappings on all of that. So the question, you know, that a lot of people, you know, would ask in all of this is really how effective has the NYSE been? Everyone who has passed through that scheme, the one-year program, there was a conversation about increasingly, you know, monthly allowance some time ago, which eventually was done. But how effective has it really been? In what ways does it develop the Nigerian youth? In what ways does it help the Nigerian economy? In what ways does it also help with the unity of Nigeria as, you know, it was, you know, started. So how would you argue? Would you say that? So I think, you know, I would agree that it has lost its effectiveness.  But it doesn't really, you know, do a lot of personal growth as much as it used to or originally, you know, started as, you know, and then also, I feel I don't agree that it should be totally scrapped because every country has, or most countries have their own ways that they, you know, imbibe some other type of training after university. I think it's in China or some other place, you know, there's some countries that you're forced to join in military or go for some type of military training after university, you know, for a couple of months or maybe a year, I'm not sure. So I think that we should find ways to reorganize, to re, you know, strategize with the NYSE, make it more effective, put people in separate, in certain sectors that would be more beneficial to the country. There's agriculture with which we're lacking, there's electricity, you know, which we're lacking, there is infrastructure, you know, and some of all of that. And so there should be other ways that we should be able to use the millions of you and I joined youth that pass through this, you know, scheme in years to become more effective, you know, to also learn, you know, more about, you know, personal growth away from whatever field that you even studied.  If you, of course, read, you know, at Greek, you could work in some other place, you know, building, you know, some other type of infrastructure that would be more beneficial to the person and to the country. And so, you know, because over time we focus mostly on oil, every other part of the country basically has not been able to develop, has not been able to get, you know, talent and skills infused into it. So that's what I feel it should, you know, should be done. The people who graduate should be moved into certain sectors and it should be monitored to be ensured that they are truly utilized and both ways it's beneficial instead of just hanging around some place for one year. So, I actually agree with you when you say it should be rigged in some ways so that the scheme at the end of one year, you know, is beneficial for both the company or the community that you're serving and the individual themselves. But regarding the effectiveness of the NYC scheme, I would say one thing that has, you know, greatly, you know, just done a lot to basically undermine the intentions of Yacobo Gowon when he created this in about 1973 would be corruption because there are people who now make a living off redeploying people. You're posted to the North and their business basically is to connive with NYC officials in Abuja to change your posting location from Kano State to Lagos and they will collect a high price and I know lots of people who do that. They posted on their WhatsApp status. Where are you posted to? Are you not satisfied with it? Come and pay me certain amount of money. I will make sure you get posted to your state of choice. So that corruption issue, that was not what Yacobo Gowon had in mind. You know, there was a civil war, there was a North and Southwest and whatever issue. So he said, I want us to be able to rebuild, to be rehabilitated, to just, he had his three hours policy and said, I want us to be able to live together. I personally was posted to Adamao State in 2017. I could have redeployed. I remember when, you know, they were distributing the redeployment form. I remember calling my parents and said, I feel at peace here and I stayed in Adamao for one year and I really enjoyed it. If I hadn't gone to Adamao for one year, I would never have understood what it means to actually be in Northern Ireland and to understand the possibility that they embody. Those people are very friendly. I don't know what I'm coming. They're very friendly. They are just so nice. They're just amazing people. I would never have known how cheap it was to buy food in the North. I would never have seen the opportunities and all the other, you know, challenges we have in Lagos. A one bedroom flat, very big apartment, 80,000. 80,000 would never get you something reasonable in Nigeria, in Lagos. So going to another part of the country, open my eyes to the realities of what other people experience. And I feel people should be able to experience that as well, rather than let corruption seep into that and begin to, you know, manipulate this and that. So I think what the government should do is not scrap NYC. It's not throw the baby away with a bathwater, fix the issues within the NYC, make it difficult for NYC officials to begin to collect money for people to redeploy. All these things, if you fix corruption, see, I think corruption is one of our biggest killers. So don't, don't, don't. No, I'm coming. I'm coming. Again, I'm not done. Yeah. When we talk about the corruption issue, also the security issue, because all those people who redeployed, they had valid reasons. Of course, I remember when I was in Adama, people were calling me every day because we had bombings here and there. They hear that, oh, in the news, there's a, there's a bomb blast or something in, in Adama, I'm safe. So yes, those people left for valid reasons because of security. So the government also needs to fix security issues. These are things that they need to tackle, not just say NYC should be scrapped. So if NYC is scrapped to say, I should not go to the North, if I have an engagement that means I need to be in the North, does that mean I will not be in the North?  So it is impossible for you to say that, um, transversing the country from one, from, from one party to the other is not going to be possible. It's, it's, it definitely would happen that a time will come you need to go to the North. So those issues of security, all those things that make people dissatisfied with the NYC scheme should be fixed, not the NYC scheme being scrapped. So I think, I think, you know, that's where you should have started from, you know, addressing some of the things. No, I have to start with how NYC benefited my life. No, no, no, no.  Yes, you know, it does exist. And I mentioned it also that people who can lobby for where they want to be posted to. But the thing is, you know, I feel like we should, you know, you should start it with the reasons a lot of people want to deploy, aside of the fact that there are a lot of Nigerians and lazy and don't want to deploy because there's an opportunity for them to deploy. There's an avenue. That's one of the reasons, there's an avenue for them to deploy. No, aside the fact that there is that avenue, and that's where the corruption comes in. The point is, when, you know, there is other valid reasons why people don't want to take that risk and go that far away from home for one year, those are where, you know, the fixing needs to start from. The fact that a lot of people also don't see the actual value. I mean, your experience, you know, might be called beautiful, but it doesn't invalidate the experience of other people who have had a very, very horrible experience with it. And so those things that, you know, people think about and say, I'd rather just stay where I am, where I know that I'm safe, where I know that I'll be of more value. Those are the things that need to be fixed first, so that whenever you tell a person, oh, you're going to be deployed to your base state, they have zero fears. They know it's going to be a full experience. They're going to be used to doing that in that time. They're looking forward to it. But if you don't fix those things, there's always going to be, you know, some people looking for a loophole where they can pay their way out of it. So it's not just the corruption. Corruption exists. Even in healthcare and education everywhere, it does exist. But if you don't fix those extra details, if you don't make a person a Nigerian see the value in the NYSC, then, you know, there's always going to be, you know, people searching for loopholes. If you don't make a Nigerian feel safe anywhere in the country, any Nigerian now, if you tell the person, oh, go on, do your NYSC cuts in that?  Eight out of 10 parents would tell you hell, no, sit at home. It's better you sit at home and join me in the shop than go risk your life in Borno State or in Yobain, some of all those places. And so those things need to be fixed. A lot of people, you know, go to the NYSC and end up becoming child rapists. You know, those things need to be fixed. Going all the way to schools where you're teaching secondary school children. Nobody really has been able to explain the value in all of that using, you know, university graduates to become teachers in some secondary schools, some remote secondary schools or primary schools in, you know, different parts of the country. That's another thing that needs to be fixed. The fact that, you know, like I mentioned that employers exploiting youth comm members, they would not hire prominent staff or they wouldn't pay the ones that they have. They would rather enjoy the benefits of, you know, the flow of NYSC members, you know, from the NYSC scheme. We see lots of job advertisements. They need an NYSC member. They need an NYSC member. Somebody they can just use for cheap labor. They can pay you 10,000, way less than the minimum wage and they schedule after one year. They know that next year or the next few months and next batches and new NYSC staff. So they keep using Nigerian youth to just fund and fill their corporates while leaving the Nigerian youth just high and dry. So these are the things that need to be checked, not just throwing the scheme out. Yes, you know, like I said, you know, I don't think it should be scrapped. It should be re-jigged. It should be reorganized. It should be become more profitable to both the youth and to the country. There's a lot of sectors in Nigeria that need hands, that need extra hands and need extra service. And I think that's, you know, those are some of the areas that they should be sending, you know, these young people to where you can learn. You can develop yourself and become B. Yeah, exactly. B, beneficial to yourself and B, beneficial to the country. The wage is currently run is, you know, very, very, you know, it's of no use really to both the Nigerian youth and to the Nigerian, down to Nigeria itself. That's, you know, what I think. The corruption, yes, it does exist, just like it exists in infrastructure, just like it exists in healthcare and in education and in the police and in the army, you know, exists everywhere. But scrapping that corruption is not really the answer. If you say, oh, you know, stop taking money for redeployments, you are really only going to be saying that people don't no longer have a choice to decide whether they want to be forced to go to Borno or not, or be forced to go to Katzina or not. A lot of people don't want to go to those places, mostly because of security challenges. How many people can travel by road today? If you deploy a person to Katzina, how many of them would go by road comfortably and say, okay, I'm heading to Katzina for NYSE?  A lot of people fear that when they are there, they might be kidnapped or they might be killed.  All right. Short break. We'll take a break. And when we come back, we're going straight into the papers. Chris Wando will be joining us this morning to go through the major news stories making headlines across Nigeria today. Stay with us.


Hello friends, welcome again to another session on polynomials and Moving forward with our sessions the series of sessions Now we have reached at a point where we can discuss remainder theorem and factor theorem So in the previous few sessions use you you'd have seen our preparation to come to this level and then now In this particular session, we are going to understand this in detail So if you have not seen the previous videos I would request you to go back and see the division method the synthetic division method and then the immediate previous video of where we have explained the The very basic Equation or relation where the dividend was equal to quotient times Deviser plus the remainder, right? So we are going to use this particular relation to understand remainder theorem now So if you'd have if you recall in the previous Previous session we discussed something of the sort that FX is a polynomial in X and It was being divided by a divisor a linear expression X minus C linear polynomial wherein we got a quotient GX and a constant remainder Rx now I'm Purposefully mentioning Rx just to make you you know feel that all these expressions which we are dealing with are all polynomials in X Okay, so variable is X So whether it is a constant or it is a polynomial if it is a constant the degree of that constant is zero You know that But at the end of the day we can say that all of them are polynomials in X, right? So this is what the relation was which we were discussing the other day and And now it's time to do a little bit of more analysis on this Other things which we learned in the previous session was that degree of FX and degree Degree of FX. I am writing like that degree of FX was equal to degree of Degree of X minus C which was one isn't it Which was one plus degree of Degree of GX that is the quotient. This is what we learned In the last last session right degree of GX Correct is what we learned and we also learned that degree of Rx in This case, it's a constant but generally speaking degree of Rx In this case Rx is constant You know we saw that when you divided it with a linear polynomial the remainder is always constant We discussed this in the previous session But generally speaking degree of Rx the remainder expression or remainder polynomial will be less than degree of the divisor polynomial Okay, so in this case the divisor was X minus C So hence since the degree of X minus C is how much guys, you know this this is linear Polynomials if this is one and less than one the only possibility is zero negative numbers. Anyways, I'm not allowed in polynomials So degree of Rx will be zero and hence it is it was a constant term correct. This is what we learned Now what is remainder theorem guys? What does remainder theorem mean now remainder theorem is a mechanism to find out the remainders When a particular polynomial FX is divided by a linear polynomial X minus C again I'm writing it so that it becomes, you know solidly you know Stablished in your mind. So you must remember this that remainder theorem is a Is a mechanism. So let me write it as RP in short is a mechanism mechanism or way or method mechanism to find out find out remainders Remainders when when Or not remainders remainder right remainder remainder Only one remainder will be found out in one division when a polynomial Poly No male again, please remember we are talking about polynomials only when a polynomial FX is divided divided by a linear linear polynomial polynomial X minus C Okay, where C is constant X is the variable right is a mechanism to find out remainder when a polynomial FX is divided by a linear polynomial X minus C or Rather we can generate it generalize it. Sorry instead of writing a X minus C. Let's write it as Any linear linear polynomial will be of the form of a X plus B, right? This is a linear polynomial. So what is Remainder theorem remainder theorem is a mechanism to find out remainder when a polynomial FX is divided by a linear polynomial AX plus B without in brackets you can write without actual without actual division. So you don't need to divide it Okay, you don't need to perform the division to find out the remainder you can do it just by using this theorem and let us see how So, let us say if if FX is divided by AX plus B the The quotient is let's say GX. Okay, so we're saying let us say let us say that that when when when FX when FX then FX FX is divided by divided by FX is divided by AX plus B Okay, then quotient is GX and remainder is Rx Okay, let us say you're dividing you're not actually performing the division But you just divide you're saying that if you divide it, you'll get these then Can we not say that by whatever we discussed in the previous sessions and earlier as well that FX will be equal to AX plus B the divisor into the quotient plus the remainder Is it it? Can we say that? Yes, we can say that right now now That means can I now say that FX is equal to A times X plus B by A So GX plus Rx, can I say that? Yes, we can so if you see this thing is same as AX plus B So I've just taken a common purposefully why what what is the purpose will you will come to know a little while later? Okay, now this is the What is this basically? This is an equation in X everywhere There will be polynomials and expressions in X. Isn't it now what happens if X is equal to minus B upon A If let's say for one specific value of X, which is minus B by A What will you see? You will see FX. So instead of X. I can write minus B by A. So F of minus B by A Okay, so you now know how to find out the value of a polynomial at any given value of the variable So we have dealt with in previous sessions. You can go and check that out as well So now if X is minus B by A I'm interested in finding the value of the entire polynomial both LHS and RHS. What will happen? So LHS I wrote in the RHS you have to write A and instead of X You have to just deploy a minus B by A and there was a B by A already Okay, then this is G and minus B by A and Plus I'm generally saying R whatever it is. Let's say R remainder, right? You can say minus B by A as well, but then I'm just saying whatever it is. It is a remainder at the end of the day Okay, remainder. So what do you see guys in this case? If you see this is coming out to be zero Minus B by A plus B by A is zero. Zero multiplied by all of the factors will Whatever is the value of G of minus B by A and A if you see this is becoming zero So you will be left with minus B by A f of minus B by A is equal to R Right, so don't we get the remainder guys? So we just got remainder remainder remainder when when FX is divided divided by AX plus B Right remainder when FX is divided by AX plus B simply f of minus B by A Right, this is what is called remainder theorem not special case Cases special case. What is the special case? special case is let's say a is equal to 1 and B is equal to minus C. Okay, and then we'll get back to our initial, right? So in that case AX plus B will be AX plus B simply X minus C right, so hence Friends if you want to divide FX by X minus C let's say the Caution is GX and the remainder is R You can write X You can leave X as well because anyways that is going to be a constant Right on constant terms of RX. So hence what will happen? So R X R will be simply f of minus B by A Minus B was our what C and a is one so f of C. So simply R is f of C Correct. Is that okay? So this is the this is what is called remainder theorem. Let's take an example and Then you know, you will be more comfortable. So if you remember in the previous Session, we had one division Okay, and this was the division. So FX was in that case FX was X cube, let's take an example.   This is what we had got the previous You know previous session, this is what FX it was This was X plus 2. This is GX and This is R Okay, and this was the divisor linear divisor Okay, now let's say this was obtained by long division method by long or the synthetic division method Which we saw long or basically by division method. We actually divided divided it Okay, but then let's say we didn't divide then what will be the remainder According to the remainder theorem. So X plus 2 if you if you see this, what is the value of A here? A is 1 and B is 2. Is it it? So the remainder will be simply F of Minus B by A is the remainder, isn't it? If you remember Just check above. We just saw that remainder is F of minus B by A. What are B and A? If you are dividing it by AX plus B, then you know, what is A and what is B? A is coefficient of X B is the constant term So in this case X plus 2. So what is A? 1. What is B? 2 So hence R should be equal to F of minus B by A. Let's check So that means I have to find out the value of F at minus B by A So mine that means F of minus 2 B by A is minus 2 minus B by A minus 2, right? So I have to basically find out F of minus 2 Now what was FX? FX was X cubed plus X squared plus 2X plus 3 Isn't it? That means we have to just simply find out F minus 2 and this will be the remainder, right? This is what it is saying. Reminder is F of minus 2 So let's find F of minus 2. So minus 2 to the power 3 plus minus 2 squared plus 2 times minus 2 plus 3 Okay, so this is minus 8 plus 4 minus 4 Plus 3 and you you see we are getting minus 5, right? Which matches with our long division Reminder, isn't it? So this is a beautiful theorem that without dividing you can find out the remainder on if for any given division, isn't it? Once again, right? So let's say if you are dividing it by if you're dividing FX by AX plus B Okay, then simply remainder is F of minus B by A, right? And for most of the cases it will be very simplified if you are dividing FX by X minus C, let's say for this form then then remainder is simply F of C because if you see minus B by A in this case if you try to compare it by compare it with AX plus B What is A guys? A in this case is 1 and B minus C So minus B by A is simply C, right? So hence R is minus B by A or F of C. So both these forms you remember This is a general form and this is a specific form when the coefficient of X is 1 and X minus C is what you're using to divide FX, okay? This is remainder theorem. We'll see some problems on this to make it more clear. I hope this theorem is understood. This is a very vital theorem. You're going to utilize it multiple number of times till your algebra journey is on. Thanks for watching the video.


Do you know? If not, you're in good company because this was the title of a song published by the Danish food administration and in the song You learned that legumes are for example beans or peas and lentils And they aren't only healthy, but actually really amazing because they need way less fertilizer than other crops like barley and wheat and Fertilizers are a huge problem More than 1% of the of the world's yearly energy consumption is only used to make nitrogen fertilizers And then we use way too much of them and they pollute our lakes and rivers So what can we learn from legumes? Well legumes work together with special bacteria that give them all the nitrogen they need and The bacteria live inside the roots in these small bumps that you can see here So now imagine barley could do the same we could save so much fertilizer But in order to engineer barley we first need to understand how legumes work together with a special bacteria and When I started my project, we knew that there are two types of proteins So big molecules in the roots that recognize the special bacteria But we didn't know how these two Proteins interact to tell the plant to make the bumps So to study that I took a small antibody and fused it to one of the proteins and then the antibody bound to the other protein and thereby we brought them really close together and Then suddenly the legumes started making these bumps although there were no bacteria around So then we knew the legume makes the bumps when the proteins come close together And then we could take that knowledge and look at barley and we found two barley proteins that could also tell the plant to make the bumps So now there's still a long way ahead of us before barley can survive without fertilizers and Engaged with these special bacteria, but we've really come a step closer So next time you pull a pea plant out of the ground and look at the roots and see these bumps I want you to remember that special bacteria live inside them that help the plant to survive without fertilizers and We can learn from that pea plant how to engineer other plants like barley so that they will also need less fertilizer in the future I Think pea plants and all legumes are really amazing, and I hope you do too now. Thank you very much


Hello and welcome to the session. In this session we will represent addition and subtraction of complex numbers genetically on complex plane. First of all let us discuss addition of complex numbers and complex plane. Now we know that any complex number is written as what is equal to x plus i eta y where x y belong to the set of real numbers. Also x is called the real part and y is called the imaginary part of this complex number. Also we can represent the complex number x plus i eta y as ordered pair x y. So on this eigen plane all we can say on this complex plane the point p with coordinates x y represents the complex number x plus i eta y where x represents the real part and y represents the imaginary part of the given complex number that is the complex number x plus i eta y. Now we will represent addition of two complex numbers on complex plane. Now suppose we have complex number z 1 is equal to 3 plus i eta and complex number z 2 is equal to 1 minus 5 i eta. Now we will represent some of these two complex numbers that is z 1 plus z 2 on complex plane. First of all let us represent complex number z 1 which is equal to 3 plus i eta on complex plane. Now for this complex number real part is equal to 3 and imaginary part is equal to 1. So we will move 3 units right and 1 unit up from original and we reach at this point let this point be p. So we have obtained point p with coordinates 3 1 which represents the complex number z 1 which is equal to 3 plus i eta. Now join op now we will draw complex number z 2 which is equal to 1 minus 5 i eta on complex plane. Now here we see that real part of this complex number is 1 and imaginary part is minus 5. So we will move 1 unit right and 5 units down and we reach at this point let this point be q. So we have this point q with coordinates 1 minus 5 which represents the complex number z 2 which is equal to 1 minus 5 i eta. Now join op now let us complete the parallelogram. Now op r q is the parallelogram. Now from original join the diagonal op r. Now this point r represents the addition of the 2 complex numbers that is z 1 plus z 2 and here you can see we moved 4 units to the right and 4 units downwards from original to reach the point r. Thus point r has coordinates 4 minus 4. So it is complex number 4 plus or minus 4 i eta that is 4 minus 4 i eta. So z 1 plus z 2 is equal to 4 minus 4 i eta. Now we can check our answer by actual addition. Now z 1 plus z 2 is equal to 3 plus i eta the whole plus of 1 minus 5 i eta the whole and this is equal to 3 plus i eta plus 1 minus 5 i eta. Now combining real and imaginary parts this is equal to 3 plus 1 that is 4 plus i eta minus 5 i eta that is minus 4 i eta. So we have obtained z 1 plus z 2 is equal to 4 minus 4 i eta. Now let us discuss subtraction of complex numbers on complex plane. Now if z 1 is equal to x plus i eta y then minus z 1 is equal to minus of x plus i eta y that is equal to minus x minus i eta y. Now here you can see in minus z 1 the sign of x and y are opposite to the sign of z 1 or to represent minus z 1 in complex plane it is drawn in opposite direction of z 1 that with same magnitude. Now let us take some complex numbers that is we have z 1 is equal to 3 plus i eta and z 2 is equal to 1 minus 5 i eta. Now we have to represent the difference that is z 1 minus z 2 on the complex plane. Now we have already drawn z 1 and z 2 on the complex plane. Now to find z 1 minus z 2 we first draw minus z 2 that is equal to minus of 1 minus 5 i eta the whole which is equal to minus 1 plus 5 i eta on the complex plane. Now real part of this complex number is minus 1 and imaginary part is 5. So we move 1 unit left and 5 units up from origin to reach this point let this be point q dash with coordinates minus 1 5 which represents the complex number minus z 2 which is equal to minus 1 plus 5 i eta. Now here you can see that minus z 2 is in opposite direction of z 2 and of same magnitude. Now let us complete the parallelogram. So we have completed the parallelogram o p r q dash and draw the diagonal r. Now this point r represents the subtraction of the two complex numbers that is z 1 minus z 2 and here you can see we have moved 2 units right and 6 units up from origin to reach point r thus point r has coordinates 2 6 so it is complex number 2 plus 6 i eta thus z 1 minus z 2 is equal to 2 plus 6 i eta. Now we can check our answer by action subtraction now z 1 minus z 2 is equal to 3 plus i eta the whole minus of 1 minus 5 i eta the whole which is equal to 3 plus i eta minus 1 plus 5 i eta. Now combining the real and imaginary parts we have 3 minus 1 that is equal to 2 plus i eta plus 5 i eta that is equal to plus 6 i eta. So z 1 minus z 2 is equal to 2 plus 6 i eta. So in general if z 1 and z 2 are two complex numbers and the points p and q represent the two numbers then by completing the parallelogram and drawing the diagonal point r will represent complex number z 1 plus z 2 and in difference z 1 minus z 2 minus z 2 is additive inverse of z 2 and points p and q dash represent complex numbers z 1 and minus z 2 respectively then completing parallelogram and drawing the diagonal point r will represent the complex number z 1 minus z 2. So in this session we have discussed how to represent adhesion and suppression of complex numbers geometrically on complex plane and this completes our session hope you all have enjoyed the session.