Transcript for:
Control and Coordination in Biology

hi everyone and welcome to miss estri biology in this video we're going through topic 15 control and coordination this is everything you need to know for this topic and if you do want that all written in one place for you then check out my a-level notes which cover all the theory for cie key terms key marking points and you've got examiner tips included there as well so there's a link below for you to help boost your a level grade but for now let's get into the content topic 15 then and it's all to do with control and coordination so in chapter 14 we saw how homeostasis occur to help regulate blood glucose levels and water potential and you can actually have a look at that previous video as well but in this video it's going through how you can also have coordination and control using the nervous system and with the nervous system it's going to be far more rapid rather than gradual which is what the hormonal response is so insulin glucagon ADHD and adrenaline are examples of hormones which act as signal molecules released into the bloodstream and they travel long distance from where they're produced to their target organs and these hormones are produced within endocrine glands which basic means a gland that produces a hormone and groups of cells responsible for secreting one or more substance directly to the bloodstream endocrine glands lack ducts and the endocrine system encompasses all those ductless glands within the body including the pituitary gland which we can see at the top just here within the brain so if we have a look at the nervous system compared to the endocrine system I've put together this summary table for you so you can screenshot it print it out and put it into your notes or maybe turn into flash cards um but you need to know the comparisons between the mode of communication so how the information is delivered electrical impulse versus hormones the speed duration of the effects the target tissues response time adaptation to stimuli regulation of functions organs involved mechanisms of actions and feedback regulation so these are all just key facts to know so I'm not going to talk through all of this you can screenshot and keep that in your notes so moving on then just focusing on the nerve system the nerve system is made up of billions of neurons these can be categorized into three main groups Sensory neurons relay neurons and motor neurons and these three specialized cells do still have some features in common so they all have a cell body which contains the organal you find in a typical animal cell so for example the nucleus and the mitochondria they have dendrons which carry the action potentials to surrounding cells and they have an axon which is a conductive long fiber that carries the nervous impulse along the neuron so if we then have a look at the actual structure we can see so we talked about some of those here's our cell body we've got the nucleus inside of that cell body this part is the axon and we can see the dendrons branching out here as well melinated neurons have shron cells as well which is shown here in yellow wrapping around the axon and they wrap around to form what's known as the myelin sheath and this is a lipid and therefore it doesn't allow charged ions to pass through it and in that way it insulates and prevents the electrical impulse from traveling the entire length of the axon instead as to jump from node to node which is know as a node of ramir and that speeds up the conductance so that's what we've got here that those gaps are called the notes of ranir and we get that action potential jumping from node to node which is known as statory conduction and that is what speeds up how quickly that impulse can travel so if we have a look at a sensory neuron these are the neurons responsible for carrying electrical impulses from the sensory receptor cell to the relay neuron sometimes also to the motor neuron and the Brain they have a long dendron which carries the impulse from the sensory receptor to the cell body which is what we can see here and there is the cell body and then an actx on to carry the impulse from the cell body to the next neuron the intermediate neuron sometimes known as the relay neuron these neurons carry impulses between the sensory and motor neurons and they have multiple short axons which we can see here and also dendrons branching off each of those and finally the motor neuron these carry impulses from the relay or sensory neurons to the affector and the affector is either a muscle or gland that is the part that carries out the response and these have one long axon and multiple short dendrons a sensory recept then these are cells that detect a stimulus that is what a receptor is and these cells are transducers meaning they convert different types of stimuli into electrical impulses there are different types of sensory receptors and each type can detect a different stimulus and here is your table summarizing the different types of sensory receptors and the stimulus they detect so photo receptors photo meaning light they detect light and that would be your rod and Cone cells in your retina of the eye Thermo receptors Thermo means temperature so they can detect changes in temperature or heat energy mechan receptors so the pinan Corpus skule and the sinus Corpus as well detect the pressure taste smell and balance as well so taste and smell a chemical balance is movement next time we move on to the actual changes that happen in a response and when there isn't a stimulus your neurons would be in resting potential state so that's what we're going to go through first when a neuron is not conducting an impulse meaning there's no stimulus there is still a difference between the electrical charge inside and outside of the neuron and that is known as the resting potential you actually have more positive ions which are the sodium ions and potassium ions outside of the neuron compared to inside and therefore the inside of the neuron is comparatively negative at -70 mols so this graph here is showing you an action potential which is what happens when there is a stimulus but this section here of the graph this is before there is any stimulus and we can see that the voltage which is our potential difference is remaining at Min - 70 MS so the way that that occurs then is there is a sodium ion potassium ion pump and this stage requires ATP for active transport and this co-transporter pump will pump two potassium ions into the axon of your neuron and three potassium ions outside of the cell that creates an electrical chemical gradient because we'll then have more potassium ions inside of the cell and more sodium ions outside of the cell and as a result of those electrochemical gradients potassium ions will diffuse out of the cell through these channel proteins and sodium ions will diffuse into the cell through their channel proteins however there are more potassium iron channels than there are sodium iron channels so we say that the membrane is more permeable to potassium ions also the potassium ions are permanently open and some of the sodium iron channels are not permanently open so as a result you get more potassium ions diffusing out than you do sodium ions diffusing in and as a result you have more positive ions outside compared to inside and that is how we get this minus 70 M volts or the resting potential so if there is a stimulus that can result in an action potential and this is when the neurons voltage potential difference increases Beyond a set point from that resting potential so our resting potential is- 70 molts but if we actually get a change that brings the voltage up to the threshold point of minus 55 molts then you will get an action potential occurring so an increase in voltage also known as depolarization is due to the neuron membrane becoming more permeable to sodium ions mean meaning more sodium ions are going to diffuse into the axon and because those have a positive charge that will bring that voltage to become more and more positive so we go from -70 up to - 55 which is more positive once an action potential is generated it moves along the axon like a Mexican wave so you'd have to generate that action potential at this point on the axon that would then trigger an action potential in this node of ran and then this one this one this one this one and that's what we mean by the movement being like a Mexican wave so let's go through then how an action potential is generated we've got our resting potential here where we've got those voltage gated sodium channels closed what that means is these are sodium channels that sodium ons can diffuse from the outside to the inside of the cell however those channels only open when there is a particular voltage whereas we have some potassium channels which are Perman opened so that's what's happening at our- 7 m for the resting potential but if there is a stimulus that stimulus causes some of the voltage gated sodium on channels to open and as a result sodium ions are going to diffuse in and that causes the voltage to become more positive now if you have a large enough stimulus that will cause enough sodium ion channels to to open to reach the minus 55 molt threshold if it's only a small stimulus that won't cause enough of those voltage gated sodium on channels to open so you won't actually get an increase in the voltage to the threshold of- 55 M volts and therefore you wouldn't respond to the stimulus and that's actually really useful because you don't want to respond to every slight change because that would overwhelm your senses so you're only going to respond if the pressure or the sound or the smell is strong enough that it does deem worthy of responding to so that it would actually protect you from potential harm now when you do get to that threshold Point minus 55 molts that causes even more voltage gated sodium on channels to open and therefore you get even more sodium ons diffusing in making that voltage now become positive and it Peaks at plus 40 mols now when you get to that point that then causes those voltage gated sodium IR channels to close but we still have potassium iron channels that are permanently open so we now have positive arms being diffusing out so going to leave the axon so we then start to become more negative again which is known as repolarization at this point we have even more potassium arm channels open so even more potassium Aro diffusing out which actually results in this overshoot where the the voltage becomes even more negative than the resting potential and we call this stage hyperpolarization where the voltage can go to minus 80 MTS and this is known as the refractory period as well during this point these voltage gated sodium iron channels are tempor temporarily unable to open so you get a very short period of time where a new action potential wouldn't be able to be generated um and we're going to talk about why that is is an advantage but for now that is just showing you how that depolarization results in this action potential and then how that afterwards results in repolarization going into that refractory period but then because of that sodium ion potassium ion pump that we talked about in maintaining the resting potential it does bring that voltage back up to the minus 70 Mt of resting so this is just what I meant by the Mexican wave that action potential is generated at this point on the axon that then jumps to the next node of ran next one and that will happen all the way along the axon until it reaches the end of that motor neuron and then we get to a sinapse so the All or Nothing principle is this concept that if the depolarization does not exceed that threshold ofus 55 MTS then you will not get an action potential so nothing happens that's the nothing part of All or Nothing any stimulus that does trigger depolarization meaning it has reached that minus 55 molt threshold the maximum voltage is always the same at plus 40 molts so a bigger stimulus doesn't result in a greater Peak a greater voltage it's always going to be a maximum of plus 40 molt because of the set number of channel proteins present and the number of ions present but what does vary is the frequency at which those action potentials are going to be generated so the larger the stimulus the quicker the frequency or the higher the frequency so this what we mean this is what we mean by the All or Nothing principle if you don't reach that minus 55 molts then nothing will happen you won't get an action potential but if you do then you'll always get an action potential and it'll always Peak at that same voltage so it's important as this makes sure that animals only respond to a large enough stimuli and this is what I was talking about when we mentioned the threshold potential earlier you have to have a large enough stimulus to reach that threshold and therefore you're only going to respond to large enough stimuli and not every slight change in your environment because that would overwhelm your senses so a bit more about the refractory period after an action potential has been generated the membrane enters that refractory period when it can't be stimulated again and that's because those sodium sodium ion channels are recovering and they can't be opened so that is important because it ensures that discrete impulses are produced an action potential cannot be generated immediately after another and that is why it makes sure that each impulse is separate it also ensures that action potentials only travel forwards in One Direction it stops the Action Potential from spreading out and going backwards and if it did go backwards along the axon that would prevent it causing a response because it wouldn't actually end up reaching the affector and lastly it limits the number of impulses and that's important to prevent an overreaction to a stimulus so how you can then speed up these impulses one way is the schan cells which we briefly talked about Shan cells wrap around the axon to form the M sheath which does not allow the charged ions those sodium ons and potassium IRS to pass through going in and out of the axon there are those gaps which are known as the node of ramir though and that results in the saltatory conduction which is where that action potential jumps from node to node and that means the action potential travels faster along the axon because you're not generating an action potential at every single position along the axon so when that impulse does reach the end of a neuron on it reaches a gap which is known as a sinapse so the copses are these gaps between the end of an axon of one neuron and the dendrite of another one and at that point the action potential is transmitted as neurotransmitters which are chemicals which diffuse across the sinapse so let's go through how that happens when that action potential reaches the end of the neuron that is known as the synaptic knob the end of the neuron and depolarization of the synaptic knob causes calcium AR channels embedded within the membrane to open and therefore calciums diffuse into the Coptic knob those calcium ions cause vesicles within the synaptic knob which contain the chemicals the neurotransmitter to move towards the cell surface membrane they fuse with that preoptic membrane and when they fuse that causes the release of the neurotransmitter by excess cytosis into the synaptic cleft which is what we call this gap between the two neurons because that neurotransmitter is only being released from the preoptic neuron we have a concentration gradient so that means the neurotransmitter chemicals can diffuse down their concentration gradient which causes them to diffuse across the Coptic CFT to the post synaptic neuron and it goes to the membrane of that postoptic neuron which has receptors embedded within that neuron membrane and those receptors are complimentary in shape to these neurotransmitter chemicals and as a result the neurotransmitters bind to those receptors once they bind to those receptors on the postoptic membrane that causes sodium on channels on that postoptic membrane to open and once those sodium on channels open sodium ons can diffuse into to the postoptic neuron causing the post synaptic neuron to depolarize and that depolarization can then result in the generation of an action potential and that has then triggered an action potential in the next neuron those neurotransmitters do not remain permanently bound to The receptors though because if they did that would result in the action potential constantly being generated in the postoptic neuron even if there was no longer stimulus there so that means the neurotransmitter has to be released from the receptor and the way that that happens is the neurotransmitter chemicals are broken down or degraded and that causes them to be released from the receptor that causes the sodium on channels to close and that is how you then don't get any more action potentials being generated and that broken down or degraded neurotransmitter can be recycled and returned back to the preoptic neuron to to then regenerate those neurotransmitters to be reused again so this response is unidirectional it's unidirectional for a few reasons first of all you only have the visle containing the neurotransmitter in the preoptic neuron you only have The receptors that the neurotransmitter binds to on the postoptic neuron and the neurotransmitter diffuses across because of the concentration gradient now an exact example of this sinapse response or transmission across a sinapse is a colonic sinapse and it's called that because the neurotransmitter is acle choline so you would go through that exact same process that we described but wherever you said neurotransmitter you'd say acetylcholine instead and the acetal choline is broken down or degraded after it's attached to the receptors by the enzyme atile Codine esterase and that breaks down the acetol Codine into Codine and acetate which then gets recycled now thinking back to when we talked about the generation of an action potential we said that you only get an action potential if depolarization reaches at least- 55 Mill volts that threshold potential so when you're at a sinapse summation has to occur to reach that threshold and summation is the rapid buildup up of the neurotransmitter in the sinapse so that you have enough neurotransmitter binding to enough receptors to open enough sodium on channels to result in sodium on diffusing in to reach that minus 55 molt threshold and there's two ways that summation can occur spatial and temporal spatial summation is when you have multiple preoptic neurons all converging at one post Coptic neur neuron and collectively those preoptic neurons should release enough neurotransmitter to help trigger an action potential temporal summation is when there is only one neuron so one preoptic neuron converging to one postoptic neuron but that one preoptic neuron will release neurotransmitter repeatedly over a short period of time to add up to enough to exceed that threshold value now at the end of your response you have an affector which can be a muscle cell or a gland and that means you'd have your motor neuron reaching a muscle fiber and the gap between the motor neuron and the muscle fiber is called a neuro muscular Junction because you've got a neuron reaching muscle so these are specialized copses which we said of form between the Mator neuron and the muscular fiber and when an action potential reaches the of the motor neuron it triggers the release of neurotransmitter aceto Coline into the Coptic Clift just how we saw that happens in a typical sinapse that acetal coine then binds to receptors but this time The receptors are on the muscle fiber not on a post synaptic neurons membrane and that then causes sodium AR channels to open sodium ARS diffuse in and it causes depolarization of the muscle cell membrane this deol ization generates an action potential that spreads across the muscle fiber membrane and into tubes known as T tubules and that gets into the T tual system so you could be asked to compare similarities between a neuromuscular Junction and a colon argic syapse so here is our comparison they both involve unidirectional movement and neuromuscular Junction is always Exciter meaning it will always result in a response whereas coleric could result in a response or you do get inhibitory synapses where chloride ARS are released um instead we've got the difference between where they connect the neuromuscular Junction is at the end of that response Arc whereas a colonic sinus can result in a new action potential generated in the next neuron and then lastly the acetol conine binds to receptors on muscle fiber membranes for a neuromuscular Junction whereas the calc binds The receptors on postoptic membranes for a neuron so at that neuromuscular Junction we said that the action potential um causes depolarization it reaches the T tual system so T tubules are these invaginations of the saral Lima which is the muscle cell membrane that penetrate deep into the muscle fiber and they ensure the rapid transmission of the electrical signal throughout the muscle fiber enabling uniform initiation of muscle contraction as the action potential travels along the saral Lima which we can see up here and into these T tubules which is shown there it simultaneously activates the entire muscle fiber the sarcoplasmic reticulum or Sr is a specialized form of endoplasmic reticulum found in the muscle cells and is crucial in regulating calcium on channels um and those cyop plasic reticulum surrounds the my fibral which are the contractile units which we can have a look at which store calcium ions so when the action potential travels along the T tubules which are here it triggers the release of calcium ions from the sarcoplasmic reticulum into the cytoplasma of the muscle fibers and this increases the calcium ion concentration which leads to the exposure of binding sites on the acum filaments which ultimately results in a muscle contraction so that leads us on to what muscles or the structure of muscles and how we get that contraction so muscles always act in antagonistic pairs which means there one contracts the other relaxes and that happens against the skeleton to result in movement of your bones my fibral are made up of Fus cells that share nuclei and cytoplasm which is known as sarcoplasm and there is also a really high number of mitochondria because for a muscle to contract you need ATP so here is a myop fibral and the myop fibral are made up of sections known as a sarir muscle fibers are made up of millions of myop fibral which collectively bring about the force to cause the muscle to contract and myof fibral are made up of two key proteins we have myosin and actin and those form the sarir and that's what we're going to have a look at in more detail so this is just showing you that SAR if I go back to here where we can see this whole or section of a my fibral and we've got sakir indicated at this point with a thin filament and a thick filament the thick filament is the myosin which is one of the proteins the thin filament is the actin which is the other protein and this time it's shown here in blue that is your myosin the thicker filament and in red here we have the actin which is the thin filament and it's just named that because they are thicker and thinner proteins so we can see here in the sarid we have that that acting on both sides and that is interleaved between between the myosin which is in this fixed position so the myosin stays in that fixed position but when a muscle contracts the two sides here with the actin slide closer together and they slide over the myosin and we can describe this contraction based on these different lines and zones in the sarir so the a band that is the section of the sarir where you have the myosin and because the myosin doesn't change position the a band will always stay exactly the same width The Zed lines which we can see here those indicate the parameters or the border of your sarir and when a muscle contracts The Zed lines get closer together so we can see that Z Line's moved in here and it's moved in there so those Zed lines get closer together that's why when muscles contract they actually get shorter and fatter cuz the Zed lines are moving closer together we then have this I band The I band is where you just have acin by itself not overlapped with any Mosin and when a muscle contracts that eye band gets shorter because the actin is sliding over the meios so you have more section where it's an overlap the H zone is where you just have meos by itself with no actin um in between it and when the muscles contract because the actin is sliding in between you have a shorter H Zone um and those are your key sections that you need to know so you need to be able to label those bands and zones and you need to know what happens to them during muscle contraction and we're going to go through how the actin slides closer together and over that myosin in this muscle contraction and this is what the sliding filament theory is when that action potential reaches the muscle we already talked about how it generates that depolarization traveling through those T tubules and it stimulates a response because it causes calcium arms to enter and those calcium ions can cause tropomyosin which is shown here in Orange is protein to move to a different position and that position that it moves to results in the acting exposing the myosin binding SES so that thin filament acting has binding SES on it that myosin heads which are these structures branching off the myosin they can bind to so once that calcium ions those calcium ions have been released and the tropomyosin has been pulled out the way The Binding sites the myosin binding SES are revealed and the myosin heads because they're complimentary in shape those attached and whilst the ADP and Pi are attached to that meos head they are the correct shape that is the myosin head to be able to attach to those myosin binding sites on acting and it forms what we call a crossbridge so we've now created a bridge between the myosin and the axin this angle that is created in the crossbridge creates tension on the mein head and as a result that tension results in this power stroke which is when the myosin head flicks it really slides that acting along the myosin and in doing so that power stroke action causes the release of ADP and Pi an ATP molecule can then bind to the myosin head and at that point it causes the myosin head to slightly change shape so that it's now no longer complementary to the myosin binding sites and as a result it detaches from the myosin binding SES on actin within the psychop there is an enzyme atpa which is then activated by the calcium ions to hydrolized that ATP on the myosin head into ADP and pi and that releas releases enough energy to cause the myosin head to return back to its original position which is known as re cocking so cocking of the myosin head is the movement of it back to its original position and as long as the calcium on are still present holding that tropomyosin out the way that whole process can continuously repeat and that will slide the actin closer and closer together until you have a full muscle contraction so the final part of this topic is looking at the control and coordination in plants and plants can't run away from animals they don't have muscles so they can't move to the shade or move to the lights like animals have evolved to be able to do this so instead they have a different range of responses to defend themselves from herbivores trying to eat them and abiotic stresses so the Venus fly trap is an example and this shows a rapid response to stimulation particularly when prey such as insects come into contact with its modified leaves known as loes and these lobes are lined with tiny sensitive trigger heads which you actually can't see in this diagram but on the red section head here that is where you'd have those trigger hairs and when an insect brushes against these trigger hairs it causes the hairs to bend generating in action potential within the plant the action potential is similar to the nervous impulses found in animals and they travel rapidly throughout the lobes the action potential spreads through specialized cells within the lobes called motor cells and these cells act as a bridge between the trigger hairs and the closure mechanism of the Trap and as the electrical signal reaches the motor cells they rapidly transport ions such as calcium ions across the membranes creating a change in turga pressure of the cells and that change in turga pressure within the motor cells causes a rapid change in the curvature of these lobes and that is why the loes end up snapping shut and as a result it traps the prey inside once trapped in that closed section the plant secretes digestive enzymes to break down the captured prey and that extracts nutrients from the insects such as nitrogen and phosphorus from their bodies and that provides the plants with essential nutrients which the environment may not contain because the poor there might be nutrient poor soil so other responses are tropisms and this is the term given to when plants respond via growth to a stimulus you can have positive or negative tropisms positive means it's growing towards the stimulus negative means it's growing away from the stimulus and plants typically respond to these three stimuli light gravity and water tropisms are controlled by specific growth factors and one key example is IAA and that's a type of Orin that can control cell elongation in the choots of the plants and actually increases cell elongation in the choot and inhibits the cell elongation in The Roots so if we have a look then at photot tropisms which is an example where it's responding to light in the shoot light is needed for the light dependent reactions in photosynthesis and the leaves which are going to be branching off the choots so it's an advantage an adaptation that the plants the sheet part of the plant will bend towards the light source a positive photo tropism and the way this happens is IAA is produced in the shoot tip the IAA is able to defuse to other cells where it isn't produced and cause cell elongation and if there's uni Al light the IAA will diffuse towards the Shaded side because unilateral means the light source is only on one side which is what we can see here in image two the light source is slightly over to the right so all of that IAA is going to diffuse to the Shaded side which is on the left that will mean we'll get more cell elongation on the left hand side compared to the right so the left side of the plant is going to be longer than the right hand side and as a result the plant starts to bend towards that light source which is useful because the plant will then get more light energy so it can absorb more of that light energy for the light dependent reactions in Phat synthesis now in The Roots we have the opposite effect Roots do not photosynthesize so they don't require light but instead it's an advantage if the roots are deeper in the soil so they can anchor in and also it helps to reach more water so in Roots if there's a high concentration of IAA it inhibits cell elongation and that causes the root cells to elongate more on the lighter side and so the root ends up bending away from the light source which is what we can see here in this animation and that is negative photo tropisms gravitropism this will then occur in the roots and shoots differently in the choots we can see that the IAA diffuses from the up side to the Lower Side so more of it's now on the lower side so it goes down with gravity that means that we get more cell elongation on the lower side and that causes that side to be longer and therefore it bends upwards and in this case it's a negative gravitropism because the plant will be growing Against Gravity in The Roots IAA moves to the Lower Side of the root so the upper side elong Gates and the roote bends down towards gravity and anchors the plant in and this is a positive gravitropism because the route is bending towards a stimulus which is gravity so plant hormones then control a range of responses in Plants such as the ripening of fruit germination of seeds and as we just saw with the IAA the lengthening of stems and when also leaves drop examples of plant hormones include orins which is what we just went through with IAA ethine which is a gas that causes fruit to ripen and gibberellin which stimulates seed germination stem elongation and pollen tube growth in fertilization so bit on gibberellin then gibberellin is needed for germination of barley seeds as an example by initiating and coordinating the physiological processes for growth when a barley seed absorbs water it triggers the synthesis and release of that plant hormone gibberellin and these gibberellins act as signaling molecules within the seed resulting in a series of events that lead to germination one of the primary functions of jellin during germination is to stimulate the production and activation of enzymes involved in breaking down stored food reserves in the seed and barley seeds store energy in the form of starches and proteins gibberellins prompts the release of enzymes such as amasis and proteases which will then hydrolize those stored reserves into smaller more accessible molecules and this breakdown by enzymes provides the embryo plant with necessary nutrients and energy sources such as glucose and amino acids to fuel the metabolism during germination additionally gibberellin promotes cell elongation and expansion which are essential processes for the emergence of that embryonic sheet which we can see in the image here and by stimulating cell elongation gibberellin enable the embryo to push through the seed coats and emerge to the surrounding soil and this growth is crucial for establishing young plants and enabling it to access light and nutrients for further development through photosynthesis gibberellin also play a role in overcoming seed dorcy which is a state of suspended growth and metabolic activity that prevents germination if there are unfavorable environmental conditions so gibberellins counteract the inhibitory effects of other hormones such as ABA which maintain seed dormancy and by promoting germination jellins help the sea to respond appropriately to favorable environmental cues such as moisture and temperature and therefore initiates the growth process orins play a key role in cell elongation like we saw and this is by stimulating proton pumping to acidify cell walls and this process known as acid growth is essential for cell elongation and expansion of various plant tissues such as stems roots and young leaves so the auxin promotes the activity of proton pumps particularly H+ in the atpases and that is located in the plasma membrane of plant cells these proton pumps actively transport hydrogen ions which are protons from the cytoplasm into the cell wall space or apoplast and as protons are pumped into the cell wall space they accumulates leading to a decrease in PH which is the acidification of the cell wo this acid ification softens the cell wall by disrupting the bonds between cellulose microfibrils hemicelluloses and pectins which are the main components of the cell wall Matrix that acidification of the cell wall increases its placidity making it more flexible and susceptible to deformation this softening allows the cell to expand more easily Under turga Pressure generating the influx of water into the cells and as a result the cell elongates that's how we get that cell elongation so that takes us to the end of this topic hope you found it helpful if you did don't forget to subscribe so you don't miss out on any 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