Cell, Protein, Cell division, Research, Cell cycle Biology: 6. Cell Division | IBornot2B
Next up, i’ll talk about interphase or before that, i’ll briefly talk about the cell cycle as a whole and then move on to interphase, mitosis also including cytokinesis and lastly, cancer and the formation and creation of cancer, which is an example of faulty cell division. So yes, moving on to the dna, we have the different kind of forms and before you can, i can talk about the different phases in mitosis. I should probably talk about the different. You know kinds of dna, so we have chromatin, which is dna, usually loosely packed and unraveled in all non dividing cells. So chromatin is the state of the dna throughout interface. Then we have a chromosome which you can see in the picture. That is, dna temporarily packaged into tightly wound and condensed versions prior to the vision and it’s easily segregated but inaccessible to transcription, and that is also what you can see because of karyotypes. When you look at the genetic makeup of a person, we lastly have chromatids during the s phase of the interface where sister chromatids separate for mitosis into chromosomes, and you can see that these x shaped chromosomes have two chromatids yeah. Moving on to the cell cycle, the cell cycle is the thing that new cells are needed to replace cells that died or to allow organisms to grow and cell division is essential, but must be controlled. So we have the m phase or the mitosis, including prophase, metaphase, anaphase, telophase and cytokinesis.
Then we have the rest of that is the interface as you can see. So we have the g1 phase, um the growth and normal metabolic roles during the first growth phase. We also have the synthesis, only s phase, that includes dna replication, which will be a topic in molecular biology coming soon and then. Lastly, we have the g2 phase and the growth and preparation for the vision and i’ll be talking about all of those in detail. The key processes are the dna, replication and organelle duplication and cell growth. Transcription translation obtained nutrients and cellular respiration are part of the are integral to the cell division. Yes, so the interface is the largest part of the cell cycle and it’s the active period for metabolic reactions and the cell performs the pre programmed tax tasks, so what it has been differentiated to do for a certain cell type. It will do that throughout the interface and be briefly interrupted throughout mitosis, and we have the first growth phase, which, as you saw, is there for growth and the normal metabolic roles. It takes place after division, the cell grows, the dna is described, transcribed and the protein is synthesized. Then, throughout the s phase or the synthesis phase, we have the dna replication in the nucleus of the dna in the nucleus. The dna chromos inc is made into chromosomes and is then replicated then. The second growth phase is the growth and preparation for actual division.
So there we have rapid cell growth and protein synthesis size for cell that prepares for this division, and many proteins are necessary for division and they need to be synthesized at the ribosomes in the cytoplasm throughout the interface and the number of mitochondria increases. So respiratory rate can be rapid to provide energy for division. Moving on to mitosis, which you can see on this graph or picture here. Mitosis is a form of asexual reproduction and it’s the process of nuclear division, where the dna is duplicated and arranged into two separate nuclei. So first we have the early prophase where the dna continues condensing into chromosomes and the nuclear envelope so kind of the membrane around the cell begins to disintegrate. We move on to the late prophase, where the condensed chromosomes appear as chromatids held at the centromere, so the center part of the chromosomes um and the spindle, the nucleic spindle. Now the mitotic spindle begins to form the centrioles move apart, which are kind of the poles of the cell. The microtubules form part of the developing spindle. Next up, there is the i think here it said as pro metaphase, but it can also be called delayed prophase. What i just talked about, then we have the metaphase, which is the part where the microtubules attach to each centromere and move the chromosomes to the equator, which is then the mitotic spindle and the process of depolymerization la um. The second to last phase is the anaphase, which is the continued contraction of spindle fibers that cause the generation of identical sister chromatids to separate and once chromatids are separated, they’re considered individual chromosomes and move to opposite poles of the cells and last we we have this Telophase, which is once the two chromosome sets, arrive, the fibers dissolve and chromosomes knee condense.
The nuclear membrane reforms and cytokinesis kinesis occurs. Splitting the cell and cytokinesis is the process of cytoplasmic division, where the cell splits into two identical daughter cells and in animal cells or centripetal cells um after the nf. It takes place after the anaphase, where the microtubule filaments form um concentric ring around the center, which furls the cleavage between the um cell and, on the other hand, in plant cells. It also takes place after the anaphase, but carbohydrate vesicles form at the equatorial plane and fuse together throughout which the cell plate forms, which is visible in binary fission and throughout all of that. The super coiling of the chromosomes takes place. So we have um the normal dna, as you know it in the double helix form surrounding pro histone proteins, making up nucleosomes and it then, throughout the mitosis, starts to cylindrically coil to chromatin fibers, where for last we have this very condensed version that can be transported And easily separated in the metaphase, we have this chromosome, so that is basically what mitosis is all about, and we also have the aspect of cyclins, which are protein compounds involved in the cell cycle control, ensuring that cells only divide as required, and it is important in Detecting and repairing genetic damage and preventing uncontrolled cell division and cyclings interact with proteins so called cdks, which are so called cyclin dependent kinases and these proteins are regulatory. They form enzymes, that direct cells through the cell cycle through phosphorylation, and this phosphorylation is first the cyclin binds and activates the cdk, so the cyclin dependent kinesis then in the second part, the cdk activates target protein to regulate the cell cycle and, lastly, the cyclin is Destroyed allowing for this cycle to occur again – and here we have the cyclin expression cycle throughout the cell cycle throughout the cell cycle.
So there is the in general in another diagram. It would show the mpf the metaphase, promoting factor where the mpf activity is directly correlating to the cycling concentration and the mpf activity is always higher than the cycling concentration and by the onset of mpf activity. The cycling concentration rises substantially, and that is also why the mitochondria concentration is higher throughout that part, not only for cell respiration, but also because of cyclins, and we have four types of cyclones that take place at different checkpoints and checkpoints are regulatory points. So for g1 phase here you can see the growth condition and dna damage. The g2 phase is the checkpoint for the state of the size and replication. If the replication is faulty and another checkpoint is at the metaphase, which is when this proper spindle assembly takes place and the cyclin types are for one, the g1 cell type, which coordinates cell growth and start of new cell cycle, the g1 rds s phase um cyclin, Starts the dna replication and promotes centr centrosome duplication um solely at the s phase, it induces dna replication and promotes events of early mitosis and lastly, at the m phase. The influence formation of spindle alignment of chromatids, which is what you can see in the concentration throughout the different phases in this diagram. Lastly, for mitosis we have the metiotic mitotic index that shows the ratio, the ratio of number of cells undergoing mitosis in a total number of physical cells, visible cells, and this is an important prognostic tool for cancer actually, and the index is calculated by dividing the number Of cells in mitosis, through the total of number of cells moving on, we have the aspect of cancer, which i have mentioned throughout this presentation, and cancer is a disease caused by growth of tumors that are known as cancer, so most normal cells undergo programmed cell death Or apoptosis, but cancer cell have lost their normal control mechanisms and divide uncontrollably, which then creates the tumor, and there are two genes involved in creation of cancer um, which are the genes that control the cell cycle.
We have for one the proto oncogen that start the cell division and the tumor suppressor genes that switch off cell divisions and um mutations can make the proto oncogens oncogenes that lead to uncontrollable cell division, resulting in cell becoming immortal and non functional. And when the tumor suppressor genes are mutated, it this switches off um the stop for cell division, which again creates these immortal and ever duplicating genes. These are affected by mutagens that modify the dna as physical, chemical, biology, biological or yeah biological agents that damage the dna and cause mutation through, for example, radiation or carcinogens. For example, when you have smoking cigarettes, you can hear about it more in detail. In my video on nicotine yeah and these carcinogens are agents capable of causing cancer with long term exposure that accelerate the rate at which dividing cells make errors, and here you can see the process of the creation of cancer, and that is at first, you have the Mutation in the formation of a primary tumor and the primary tumor can either be benign, so it’s, harmless and doesn’t spread and doesn’t cause this vascularization. But if it is malignant, it is harmful and it causes this vascularization, which is the formation of capillaries. Throughout these cell groups, which causes it to spread and at the um at the process of metastasis, these new capillaries provide root for malignant cells, to break away and trace to other transfer to other parts of the body and start new cancers.
And, as you can see here in the detachment and intra physician, this malignant cell transforms to the extravasation, which then call is the invasion of a cell group forming a secondary tumor, and this cycle repeats with the vascularization of the secondary tumor and ends up becoming cancer. In the last four, so this was my presentation on cell division, and this was the last topic of um cell biology as a whole.