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so our bodies have approixmely 210 types of cells . so our bodies have 210 types of cells in our boyd. 210 types and 100 trillion cells total. tracniption at the level of organism we must understand at least 210 differne pattersn of trainciptnt her must be 210 differnet set sof genes. there are 100 trillion cells in adult, cancer cells coem from mtationsing enes and it start off in normal cells and pick up mutaiton and it takes six to seven mutaiton in differn cellt oes 

there are 210 cell tyeps in humans and each has its own patteron tranciption and has its own set of genes that turn on. and the other gnees turn off. so remember there are 210 types of cell in humans and a set of genes that are on and the other set are off. tranciption at the level of organism we must understand at least 210 differne patterns of trnaitpn ther emsut be 

so because there are 210 different cell types and eahc one has its own patter of trenaciptin and genes that are one, we have to understand at least 210 pattersn of tranciption tand sets of genes. 

there are 100 trillion cells in adults . fancer cells fceom from mutaitons in genes. so there are 210 differnet cells in the humans body and they have thei ronw trnaciprtion and set of genes and there are 100 trillion cells , and so cancer cells come from mutaiton in genes in cells. So it can take up to six or seven mtuaiton in differen cell types to give to rise to differnet cacners. 

it can take up to six or seven mutaiton in dif cell types to give rise to different cancers. cancer cells are derived from wild type cells so if u have 1000 trillion chances to cto get cacner there are 100 trill cells in adult cncer cells come from mtuation in genesna dit starts off in normal cell and pick up mutaiton it takes szit os even mutaiton in different cell types to give rise to dif cancer. 

sooo

there are 100 trillion cahnces to get cancer

whatw cells ned to do to be part of tissues and organ, di cell have dif shapes, clel what clle sneed to do to be part of tiisues an dorgan, dif cells ha

what cells need to do to be part of tissues and organs, different cells have different shape, cells in nose aye enad lungs have differen shapes. 

different cell have different shapes, hoe do cell sabot the shape they have. we dont know but there are mocluels that give the clel its shape, therethe second 

there are moelcuels that give cel its shape and these cellshace to stick to eachother thorugh cell adhesion, these cells in your nose forma betrreir between inside and outside and keep things from moving into your body that uou dont want in uyour body so the cell sticks gvery tightly this si cell adhesion there is also the Extracullular matrix. 

There is the basal lamina which is a set of protein secreted by the cell that basically makes up a solid structure that cell can stick to and so part of the cell adhesion is ….

these cells in your 

this is cell adhesion. 

there is the basal lamina whihc is a set of protein secreted by the cell that basicallt makes up a sturcture of cells that can stick to it and so part of the cell adhesion. 

neurons and rods cons rouch oand and arrange ina. wiring arrangment to send electrical signal to eachother that is formeing a cell adhesion. cell ahdeison is cricial for buidlg uour brian. withina tissue cellsa rein social contex, theya re always talkign to eahcohter, tissue homestasis we are all the same shape an size thoughout life, we dont chagnea ll the time, tehre are atisieus that are dying all the time so tissue hoemisns 

there are 210 cell types in the humans body and there are a trillion cells that come with those cell types so that means there are 100 wtrillion chaces of getting cancer . a cell to beocmeo canerous needs to go through six or seven mutations. 

Cells are held togehter by cell adhesion. The basal lamina is at the bottom and it holds the cells 

there are different cell shape and funcitons for each cell . The basal laima makes up the extraceullar matrix. 

cell adhesion, then there is tissue homestssis where basically cell tissues die and are actively being made at the same time to maintin.. 

tissues are formed from cell adhesion. cell ahesion is needed to build our brain, cu it holds neurons, rods and cones. 

cell adhesion is needed to buikd our brain, it holds neurosn rods and cones. cell adhesion i used to hodltissues, tissues are dying all thent ime so tissue homestasis is balancing cell death with cell birth 

the tisseuare are dying ying all the time so tissue heomstisis is to balance clel dewaht with cell. 

an example is the skin tissue, at the top layer is dead and we have to constabntly replace them. if we cut ourselfs witha. knif, we cut into our skin so then the skin has to repalce those missing cells and divide faster. If we mess wiht a knife we cut into our skina nd then our skin has to replace thos missing cells and divide faster to reparie them . This as well has a singlign mecahnsims 

So where do stem cells comes form? stem cella re cells that divide to give rise to all the other cells that make up the tissue. There are singling mecashims that is tissue homestsis. the stem cells are cells that divide to give rise to all the other cells that make up the tissue, stem cells are realitvley undiffernated, whena stem cell divises it gives rise to two cells one of which itself a stem cell that arenws. so stem cells divide to give rise to other cells that make up that tissue. therear esignaling mecahnsims that are going to 

stem cels are undifernated and dideve. and when they divie one becomes a stem cell to keep the supply of stem cells constant and th ohter will become spealize an undergo idfernation and no longer stme cell. his is alled terianl differnation cell cant divid eno more. So once it reaches its end of differnation it cant divide on more. 

stem cells are undifearted and dive and when they divide onebeocmes. sstem cell and the tother becomes a stermianl diffeanted cll that cat divide . it takes mutliple steps to beocm a temrianlly differante dcell from a stem cell.

so there is symetric and asymetric cell diviosn. so there is a difference. 

it takes mutliple steps to become a temrianlly differenated cell froma. stem clel. there are two types symetir candividion and assymetric. 

when a stem cel divides it give rise to two clel one of 

there are two types differnated and undiffernated , whena. stem cell divies it gives rise to two cell on of which itself a stem cell that arenws the supplies f stem cells os we alway s. 

symetric is when the produce divides and its smetric it makes two of the same cel and asymetri cis different,. symetric dividion is that the cell diviees and it makes the smae clel wtype and assymetric maeks two different types . 

what are transient amplifying cells that are the ones that the are amplified

transit amplyfing cells are going to apkify and make more , adult stem cell five rise to cell withing a parituclar tisuse os blodo cells can make bdiffernet blood cells not muscle or neuron cells. oftern but not always stem cells are located in a particualr place in the tissue, 

stem cells are located in a particualra place in tissue, in the skin they are 

adult stem cells cane make cells that are within the same tissue while emrpby stem cell sige rise to any type of cell in the body, they cane make any tyep of cell and they are plurpotentit, and adult stem cellar emultipotetn, Adutl stem cell give rise to cells of a particualr tissue but multipotentn an pluripotentin is emrbuocn giving rise to different tyes cell of dif tissues. in stem cells are locate din a paritcuel place in the tissue, In skin tissue they are in the niche and are always staying there, and then the different cell move in a partcualr pathway, cel movment, so cell diviosn diferentation and then omvemtn to proly build the skin the audlt stem cell is lmutliptot aso in skin the stem cells are in the niche where they are going to make diferenated cells and then are going to move them to the specific spto they need to be, 

emrbonic stem cell are plurpotenti they can give rise to any tep of cell in the body, we can take emrbuoc stem cell in different culture and differenat tem them into a new organ. so remember that the cell divises, difereitaiones and then moes. adult stem cellare multipotentn and he emrbonic are pluripotentn. 

so proprites of cells within tituse, they have to adport a shape carrut expression set of genes, and carry ou funciton, so they ahve to adort a shape, differnation and carry out the funcion of the genes, and replace dead and then repace them and then also adhere to eacher and communite through cell adheiosn 

the purspeo fclels within tissue si the adopt shape, differnate, replace old dead cells, and then carry out fucniton of the genes expressed, and also cell adhesion, there are four globular reposes to suriveve, divie, die, and differentate  there are growth factors like mitogens and cytokines….

growth factors are a braod catefory of singling mocluesl by they are EFG epidermal growth factors. 

so there are grwoth factors that tell a cell what to do . like mitogen and cytokines. Mitogens and cytokines are isnging mocluesl that tell a cell how to communicae. there are grwoth factorst that tell a cel to suvive, divie, differnate, anddie. 

SDDD

there ate mitogen. and cytokines that are growth factors/ singing mocluels. cytokines are singlimg molcuels for the immuen ssystem. if we arecieve addition singls that can cell cells ot divie diferatnio or die. cells can also die withouth tproper signals and they go through apotosis. this occurs udinr gnormal dvelopmentin ealry dvelpment think of a mouse paw, they have webbed digits. ealry in eovlution organism that came before the mouse have webbed paw dgist. there are delopmental pathways that follow f

in early dvelopment of mouse paws they had webbed paws. this is because of evolutionary pathways, the mous started off wtih webbed digist and to get ris of thse webbed digist the clels hav eot underog apotsis. this happens ebcause the 

the webbing dies when the cells undergo apotsis and die, the cell die througha potissi when they dont reive singals but thate are also signals that dirign devleopment tell speicif cells to die. so mosuse are gettig singals that sya kill of the webbed cells to make indpending digits. same thing tadpoles that are going to be grog iwth them the tail lels are ogign to die and then reyclrt tha tpatierly to beomc a full aud 

apotisis can occur duirn gnomale devlopment and cellualr dmamge like dna dmamge, clels ar emsalle and hav erepair mecahnsims, which dag e to dna ehppaens all te tiem dna ca react iwth water in such a wa u can lose a coupel cbas epairing. 

the cell cycle machiner is desinged to prote ur dna and trmait ur dna to the duaghet ecells, clels have mechaims that meausre the amounf of dmanage dna na di fits low temachienry will fix it and if high the clel will make i go through swereslide. 

so clels either need the right isnal or nosingal in order for them to die. there is machienry that detecs how much damange has happened on a cell for it to be comanded by the machinery to die. and if ts low it will fix it and if its too high it will kill it. why do cells need to singal jsut to surive this is becaue there a singal that keep the part in the right plae. so skin ellare pushed into themuscle cells when uget vavccinated a ball of skin do not get mad einmuscel because skin cells isngl other skin cell and if a skin cell ends up in themuscle its not getting the right isnal so its not going to divie and it is going to die. So we need singals to surtive because it ensure that the cells stay int he right palce and whn it happens tobe in thewng placeit isnt going to get the right singal there it is not going to suvie. 

If your suvive and not divind ur 

surive not dividne 

and dividne not just surividing, so ginsa trnadufion pathwas that turn soemting on andtu unosmethinf off. so

ia skin cell ends up in the muscle its not just getitng the righ sinals itnot going to divie and not jsrinve. i

stem cell undergo sel frenwl to genrate a stem cell and ap rticular difernat cel a tnrait eampyed aclel and wthis is the liange of a cell. If i sht pathway that takes for it to fully differnate. cancer that are properesi of cecner cells, theyr apidly dive, and when theyre not supose to meatsis ksin cell sned up in the brain and they travel? u got cells that divie when theyr enot suppose to and they gain mobiligyt to crawl out of theblodd vessel and into tissues. thsi si cell motlityt. clel know what tisues theyre in , but if u have a cirnma u have a tissue in u rmuscle 

cancer what ar ethe properies of cance cel? tehy rapidly divie and when theyre not usppseo tot meatsisi si whena. skinc ancer clels end up in the rbain

cancer cell gain the abilityt o walk out of the blood vessle thsi si an exaple of cell motitlity. . half mark of cells i inaptriotate growht, metais and ivie in new tissue to form seocndary tumors. cancer what are the proepro of cance cells, rapidly diving, and when theyre not suppseo to skin cancer cells endignup in the brain 

why do cell ned tisngl to just siive is because they keep eveyrint in the righ place and skinc ells are pushed int othe muscle because u gotvained it wil ensur ehta ti tides beuca sei f a skin cell ends up int he muscle skin doesnt develop there. that is not good and tere is machienrty to fix shit.lol. 

cancer and proitoes of canc eclels, the hall mark are thera er tehce

ther eis cell division, emtasisist na didive into tnew tissuet of orma s eocnadyr tumor thsi si a defec tin singling, there is division, seocndyar tormo through mesisi 

cance cells are growitng pradly and how this rate of dividion is comared to mreal. 

So cancer cel propeties of canc erllf

there are cance cell proptei lie division, metasisits and secondayr turmo. 

canc erl clls are growign rapidly and how fast this rate of division is compred to nroaml divison, think aout cell divison during emryoss . 

hall makr so cancer cells, innparopatie growth, continut eot divide when they should, metassit break away and mvoe to toher tissues, tivide in new tissues to form a secondayr tumr. they divide when surrounded by cells that are not normally theirneighbors. 

ther eis divison, emtasism and secndary tuor mformaiton  

cance cells grow rapidly and how fast this ris is comapred to rnoaml divison, emrbyogneis sudirn the non motnsh , look at a mass and ask. 

early develop is faster in division than in audlts, so its not surpiused htat cenruos three poudn tuor occurs over the cours eo fone ear. exnpus is a gro that lays an egg that is ferzlied externally and then the mom will go and fetlize, and as  result divison, developemnt is fater to preven ti from begin it from being eaten by a prey. so in XENOPUS  - the mom will lay the egg and the dad will fetilize it but division and dvelopment is fast to prevent prey from it it. at ten hours there will be thirty thousan cells 

zenupos blastocyte stage, the aciton part of the egg is atht eotp , the cells are health toghet in deads. the cells are held togehter in sehets , sheets of cells move togehter as a whole sheets are two cells thic kso the top oart of the cell areheld toghet erin sheets. and hese shets move otgehter a s ahwol these are two cells thickeness. the sheets of the cell are going to move down and around and up isnde the cell,, 

so the sheet are going to be held togehte rby cell adhesion adn they are going to form the baby the sheets are going to mvoe down and around o . so atht ebalstocyte stage of the developmeing xenopus the cell sheets are going to move down and around to start to form the xenopusthey are going to move down and arouna dn up inide the ege, the dorsal lip is where isnlginc enter happens. The dorsal lip is wher singling center happens. We end up with three type sof cell those are going to the endo. 

so the zenpus moves down and around and froms three tissue types, the ecot,medo, and endo derm. tjened derm make up the lining, the meso derm wis the stuff betweem, and the ecoderm i assume the skin. 

So again the cells are held togehte rby cell adehsion in shets ant ehyse are oging to move down adn aroune ot gernet eht inside endodrem, outside ectoderm, and the middle mesoderm. they are goin to generate the head and til end of the cells. so the shett so f the cellare moving down and around 

now we are forming the neural tube which is down’

the neural tube is going to form through the movemnt of sheet sof cells. so from the ectodemr the neuarl tube is made, the ecotderm formign the oustdie are going to invaige and fod ina dnt he nural tube will beocme the psinal ord.e r

so we are forming the nuerl tube form the ectoderm, the ecotderm is going to fold inward, inavginate and then make the nrual tube. 

therea re many aspect od velopment converint hseets of cell to tubes als, tubular solid,so the ecoderm te hrnaul 

there are may aspect of devleopemt like ocnering the sheets of cells into tubes, balls tubular solid strucutre, brian and heatr, are baically a hball, cell shape ocnsieration and what gvies the cell its shape.  so the cell sheets have to beocme balls, solid strucutres lie t brain ehart and a ball, cell shape ocnsideratn and what give the cell its shape. the cell sheets beocme a ball or tubes like the heart, the brain iiiiiiiiiiii

so bascially know that the shets are going to move downward and then around and then theya re going to form three tisseus, meso,edcto,endo derm . the ectoderm sig oign to inavinate inward and then make the neurl tube and then these sheets are going to also form balls or tube like structures in order to become heart, and brain. u might think that the shape a 

u might think that the shape has something to do with the lipid bilyater that makes up the palsma membraen ebacuse … the shape ahs somethign to d witht he lipid bilayter that makes up the palsm amembrne abeucase is th oustide of teh ce.. 

u might think that the shape has something to do with the lipd bilyaet tha meks up the palsma memrbena cause that is the outsid e

U mgith think the shape has somethign to do with the lipid bilayer because it maeks up the plamsam mebrane becuase that is the outside of thec ell. if u prufied lipds they form l

lipids are fluid and mvoment if u pule a hoe int he mermbat eh lipds flow and mvoe and fill the whole it also allows protient o flour aourn becaue thay eare so fuid they cannot dicatat he shape of thecell.  

If we take tweezeras and pull a piece of the memrbaen it doesnt distruct the shape so its not about the lipid bilayer . its not the palsma memrbena that is going to give it the shape isntead it is the fcytoskeligo filemtsn that act a sbeams that dictat the shape of thec ell. So is the shape of the cytkesting tha tdermisnt eh shape. Many think its the lipid plasma/ the lipid bilayer butecause it is so fluid it is not possible instewad we all know that it is the cytoskelogn fallments that give cell its shape. 

cell motlity. it a part of the cytoskeleton aspect. 

so there are three types of chemotaxis that contributes to cell motlity. s

so there is cell motlity chemotazis is the movmen of the clels based on the chemicals oarund in/food aorund it. so it will crawl to wherever food is at

so remember that chemotaxis is basscialy wher ehte cell will move towards the food is , it will crawl depeodning ont he chemical/food around it/ 

there is also macrophage migration where it moves left and right, basicallyt cell pushes the memrbane forward and it iwll nail it and , and contract . so the memrbena cleled the lamellipodium gets fushed forward, nailed down intro the EXM and then the rest will contract like a like a muscl that is inside that are going to pull the cell body fowrad. there are protein with trandmembre domains that are going to anchor a protein to the palsmemmrbena thsi si at pe of domain int eernal the mroe ocmpelx and orgnaim is the mroe dif combaitno of domaint hat is going to come togeher into the protein. we remo complex than works and we ahv emore domaisn. we dont hav emore gnees but we hav emore complex domins trucuter.s 

recap tf23a is a tf that contain sinz finger domain and ther ear eninv opies , it allows zine mocluels tobind and eahc domain will bind to three base pairs od ana nd this set of nin domainsbinds stwenty seven base piars odna colelctivley. antibodes alo have these odmain but theya re IG repeated domains that are oval. overla tniboes hafve 12 IF odmains. some rpotins are made up fo multipleodmains, theer is the epidermal growth facto is small and the

more xomplex organism ahve cmoplex domains but not more genes thatn simple organism.s its jsut more domains same amount fo genes. 

so there are 210 dif kind of cels in humans so we have to have at least 210 di tranciptioanl programs, we have a lot mre tf tat

because there are 210 dif kind oc ells in humans ther eneeds to be at leawst 210 di tranciptal programs. we have a lot more tf tahan simple organism because we have to turn on/off more stets of gene and so many of these eurltouc tf are made u portien that have di combiatnion

so we have 210 dif kinds of cells in human and this means we need 210 tranicpitoal programs. we nee dmore tf that simple organismbecasue we have to turn on’pff more sets of genes and so many of these ruatoic tf are made up of protein that have dic ombaitnion. wone way to gernate diveristy is by putting togeter alot of domains and uilding moduler genes an protine b mixing and amthcing di comabtiaotn od iamins eahc domais liek 

we need complex tf and more di because we need to turn on/of more sets of genes. many euartif tf are moduel protein composed of mutliple odmains,ea ch domain has a speicif fucniotn one wayt o gernate gena dn gproitne diveristy tthrough mixing and matching differne todmains to gerenate gene divideri and protein diviserisi sty mix and amtch did omains creading moduel prpteins, each domains fmaily like home chorm brom set sh3 an dhs3 ahsar eidmisalrsturjc tbnut not can ceove speizlie roele. s

the process of building new gene so radding new domains is th exiwsit gene happens through exon shuffling. the provess of building new gnes o radding new domains is done thouhg exon shuffling. ezxon shuffling occurs when exons from two dif genes get combined, tupically throuhg an accidnet and abrak and reigjoigj thsi profess only jappens in euarltones not in prokaryotes ebcause pslifnc happing in euarlptes, so exon fhusslfin occurs wheme xons from two di ene get combind througha cidnetl dna break and regjoing this happen sinearulteos and not perifna because pslicng only jappens in euarltoes, prokatue dont have introns os ciding sequenc is ocnitnous. a nd adna brack would dtry the gene funcion in euarltpn the genes are introns and they are long so whe exon shufflinghappens withing introns it shuffles iwhtou druptitn h eiaodn fram.s so exon shffling is the way we can make di f gen and protein with dif domains ebcause but it maily hapepns in euarlotesbeucas eprokayote sodnt have pslcing. latienra splic allowns one or more gene to produce mutlipl verisons. so we ca 

so we got eoxn fdhslain n lrnwien alpi wzona hdidldin ia hocinf nw nriwe wzon doem ponw fwnw ro norhwe NS RHW Lrwneiwnc palixia ia swlrinf wzona doem. FWNW RO Mkw iaodwmea ns akip swrin SOMina 

a tupic utakltnejgeje a aocidng reigon aprotien one o fmore nehcanre. 

even skipps gene is dorpusl is a experssed in seven strupes coresing to the odd number bodys emgen of the larve, even gene has sevne enhancer eachr epsoe; for one strc eonl one enhanver needs to be ian agive

first hour refresh on topic 1 

so understand that when a polymer is homeogous this means that they are able to have usbunits that are chwemically the same and they are going to be 

the polymer is homoegoiusn meaning that the subunits are goint o be chemcailly the same therefore that means that the addion and the removal is the same. so the point of at hydrolysis is to change the polymer from homgeous where the subuntis are the same to the polymer being ends chemically different. so in order to make a filemnt or a polymer there eneds to be no need required for atp orthere fcan be adp or amp PMP in order to make a polymer. the monomer is infroamted into fielemtns.

so the rate of adding and removal is the same. so what happens to amke it chemically different we are going to take a moomer all monomer that are g acitn are ogin to add a atp to the polymer and what happens is that it is goihng ot and because the rate of hylossis is lsower than the monomer adding this means that another t monomer is going to be added to the poloymer before it can hdyrlosisze and it taeks six to sevven t polymers in a row for it to be beocme d actin so that is why we have a large amount of adp at the polymer. 

remmerb taht GAP was the Once that covered ras gtp to gdp but it was a shitty gtapse therefre RAS is a losuy gtaase it needs \

RAs is a losy gtpas ras is a losy gtaps therefore it needs GAP. and so then that means that tactin monmer is a losyt atpas  not a gtpase it is a atpase that is glsowly hdyrloizng gform atp to adp once the polymer they rapdily hydroz to tapt to adp so in effect the filemtns is acitn liek apse action protein is acitn like ras once the monoemr, get on the flimer they ill get atp to adp. get on the filmernt 

so t actin or the moomer is a shitty atpase. just like rase sua s hitty gtapse which in turn needs gap. rthe rare ot poluner we start with acitn at dif concention adn . 

so looking at the graph lets about about the E the misn sis si at the psotive simeaning tnaen tht is it going to grown . the ra