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PPT On The Cell Cycle

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Published in: Biochemistry | Biology
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Cell Cycle, Where do find the DNA, Cell organelles, Mitosis etc...

Omer / Abu Dhabi

10 years of teaching experience

Qualification: PhD Student

Teaches: Science, Arabic, Biology, Chemistry, Biomedical Science, Pharmacology, Molecular Biology

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  1. Molecular Pharmacology course lecture No.l Cell Cycle Dr.Omer Yahia Elhussein B.SC. Pharmacy. M.sc. Molecular Medicine.
  2. WHERE DO WE FIND DNA?
  3. a) Plant cell Large central vacuole Tonoplast Chloroplast Cell wall b) Aninul cell Mitochondria Ribosomes NLElear envelope NLElear pore Chromatin CentriOles Rough endoplasmic reticulum Smooth endoplasmic reticulum apparatus Cytoplasm Plasma nwmbrane .00 e. Peter J. Russell, iGenetics: Copyright@Pearson Education, Inc., publishing as Benjamin Cummings.
  4. Cell and Molecular Biology Eukaryotes: (meaning "true nucleus") are organisms with cells within which the genetic material (DNA)is located in the nucleus. Nucleus: is a discrete structure bounded by a nuclear envelope . It is selectively permeable and has pores about 20 to 80 nm in diameter that allow certain materials to move between the nucleus and the cytoplasm Chromatin is the stainable material in a cell nucleus: DNA and proteins. concepts and experiments 6 edition page 10
  5. xnogv ON 00 XVHB\ DIXÄNÄ91dÄ
  6. ACTIVE CHROMATIN Bi•fig ste fa ruesscr Transcnotms AC leg. Sing corrolex) DeaceMaton Corwessor e S'AT/ DeaceMated rustores INACTIVE CHROMATIN ksta-p Histones and nonhistones are two major types of proteins associated with DNA in chromatin. Histones: are small basic proteins with a net positive charge that facilitates their binding to the negatively charged DNA. Five main types of histones are associated with eukaryotic nuclear DNA: HI, H2A, H2B, H3, and H4. Nonhistones : Include proteins that play a role in the processes of DNA replication, DNA repair, transcription (including gene regulation), and recombination. o A number of anti-cancer drugs (e.g., Zolinza) are currently being tested that act by inhibiting HDAC enzymes . Trnscrwtm• k3K9 mettyW:n e. S.LQT/ Deacetøated histores Cell and Molecular Biology concepts and experiments 6 edition page 520
  7. Ploidy Diploid MEIOSIS Haploid Ploidy : is the number of copies of chromosomes. Diploidy: Presence of two copies of genes per cell, one from each parent. Haploidy: one copy of each gene per cell rather than two as in most eukaryotic cells Aneuploidy: A condition in which a cell has an abnormal number of chromosomes that is not a multiple of the haploid number. Aneuploidy (Photo) chromosome 21 trisomy in Down syndrome) Cell and Molecular Biology concepts and experiments 6 edition page 596
  8. WHAT DO YOU KNOW A BOUT MITOCHONDERIA?
  9. Mitochondrion Mitochondrial DNA and genes dine D Mitochondrion is inherited maternally. It has an Important role in sequestering and releasing It is responsible for cellular respiration and energy production. It carries important biochemical reactions (e.g. aerobic glycolysis) It mediates intrinsic apoptotic path way (Picture)A premature-aging phenotype caused by increased mutations in mtDNA. T. Strachan, A. Read - Human Molecular Genetics 4ed(2011) page 258
  10. Mitochonderial DNA vs. Nuclear DNA TABLE 9.2 THE HUMAN NUCLEAR AND MITOCHONDRIAL GENOMES Number OF different DNA molecules Total number of DNA molecules per cell Associated protein Number of protein-coding genes ofRNA genes Gene (Ensity Repetitive DNA Transcrip tion I noons Percentage Of protein-coding DNA Codon usage Recombination Inheritance Nuclear genome 3.1 Gb 23 (in X-X cells) 24 (in XY ceils); linear varies according to plcidy; 46 in diploid cells several classes of histone and nonhistone protein -21Æcc uncertain, but >6COO —I n 20 kb but great uncertainty more than of genome; see Figure 9.1 *nes are Often independently transcribed found in most genes 61 amino acid c"ns plus three Stop at least once for each pair of at Mendelian for X chromosorTp and autosomes; pate mal for Y chromosome Mitochondrial genome 16.6 kb one circular DNA often several thcusand copies (but copy num ber varies in different cell types) argely free of protein 24 very little multigenic transcripts are produced from both the heavy and light strands absent 60 amino acid cc,dons plus four stop codonsa not evident exclusively maternal T. Strachan, A. Read - Human Molecular Genetics 4ed(2011) page 260
  11. WHEN DO CELL DIVIDE?
  12. •Gl Phase: cell growth and progress for mitosis. • S Phase: DNA replication and chromosome duplication. •G2 Phase: cell grows and carries out normal metabolism, organelles duplicate. M Phase: Mitosis. How cell cycle work Cell and Molecular Biology concepts and experiments 6 edition page 261
  13. Stages of mitosis • Interphase: Technically not part of mitosis, but rather encompasses stages Gl, S, and G2 of the cell cycle which prepare the cell for mitosis. Prophase: Chromatin in nucleus condense; nucleolus disappears. Centrioles begin moving to opposite ends of the cell and fibers extend from the centromeres. Metaphase: Spindle fibers align the chromosomes along the middle of the cell nucleus. This line is referred to as the 'metaphase plate.' Anaphase: The paired chromosomes separate at the kinetochores and move to opposite sides of the cell. Motion results from the physical interaction of polar microtubules.
  14. Stages of mitosis (cont.) • Telophase: Chromatids arrive at opposite poles of cell, and new membranes form around the daughter nuclei. The chromosomes disperse. Cytokinesis: Results when a fiber ring composed of a protein called actin around the center of the cell contracts, pinching the cell into two daughter cells, each with one nucleus.
  15. Mitosis Mitosis is the process by which a cell duplicates the chromosomes in its cell nucleus in order to generate two, identical, daughter nuclei. It is followed immediately by cytokinesis, which divides the nuclei, cytoplasm, organelles and cell membrane into two daughter cells containing roughly equal shares of these cellular components. Mitosis and cytokinesis together define the mitotic (M) phase of the cell cycle. Mitosis is a normal cellular process necessary to sustain life, but its deregulation in one form or another is found in all cancer cells. Mitosis can often become abnormal by the change in, or absence of, the normal cell cycle checkpoints.
  16. CELL CYCLE REGULATION
  17. Cell cycle checkpoints Cell cycle checkpoints are points in the cell cycle which act to ensure correct transmission of genetic information during cell division. These checkpoints look for abnormalities within the cycle, specifically chromosomal aberrancy. Checkpoints take place towards the end of each phase of mitosis and must be passed before the cell can get clearance to enter into the next stage of mitosis. If errors are found during checkpoints, the cell acts quickly to correct them, arresting cell growth and not proceeding with mitosis until the error has been fixed. If these errors cannot be fixed, the cell normally undergoes apoptosis, or programmed cell death.
  18. G7 'o COE G , qeiin Cell cycle control Peter J. Russell, iGenetics: Co Cell cycle check points t@Pearson Education, Inc., publishing as Benjamin Cummi a) B) C) Cell cycle shows 3 major check points : Gl / S check point : (restriction point) Is environment favorable ? G2 / M check point: Is all DNA replicated ? Is environment favorable ? Metaphase to Anaphase transition . Are all chromosomes attached to spindle ?
  19. Factors regulate cell cycle Cyclin - dependent kinases (CDK): enzymes that control progression of cells through cell cycle. Cyclins : are proteins required to activate cyclin dependent kinases to form an active cyclin-CDK complex (e.g. MPF ) APC/SCF: complexes: they are two classes of multi subunits complexes that function as ubiquitin ligasis . These complexes recognizes the protein to be degraded and linked it to the polyubiquitin chain , that ensure their destruction by Proteosome Cyclins:(named because their concentration increases and decreases in a regular pattern through the cell cycle)
  20. Check Point Regulation Cyc&l D cyclin E 0+9 E2F tums on for DNA s Cydn A Cydh A At the GltoS checkpoint, two different Gl cyclin Cdk complexes form, resulting in activation of the kinases. The kinases catalyze a series of Phosphorylations of cell cycle Control proteins, affecting the functions of those proteins and leading, therefore, to transition into the S phase. FRB: Retino Plastoma Protein. It is a tumor suppressor protein associated with a familial (inherited) eye's cancer Peter J. Russell, iGenetics: Copyright @ Pearson Education, Inc., publishing as Benjamin Cummilvs.
  21. How do check points prevent cancer ? E2F Entry into S phase is blocked when there is unrepaired DNA damage. Irreparable damage leads to apoptosis. Within S phase there are additional checkpoints at which DNA damage prevents new origins of replication from becoming active. is a tumor suppressor protein; have a molecular importance in many cancers Peter J. Russell, iGenetics: Copyright @ Pearson Education, Inc., publishing as Benjamin Cummivs.
  22. TO BE CONTINUED... 15 MIN, BREAK
  23. CELL CYCLE AND CANCER
  24. What is Cancer? Cancer is the deregulation of normal cellular processes. Cells that have been transformed tend to proliferate in an uncontrolled and deregulated way and, in some cases, to metastasize (spread). Cancer is not one disease, but a group of more than 100 different and distinctive diseases. Cancer can involve any tissue of the body and take on many different forms in each area.
  25. Continue..... Cancer cells become deregulated in many different ways. One way: Mutations in one or more mitotic checkpoints allow the cell to move from one phase of mitosis to another unchecked. Another way: Mutations in cellular machinery itself so that mitotic errors are not properly detected/repaired, and the cell is allowed to move through mitosis unchecked.
  26. Continue..... The cell is allowed to move through the cell cycle and grow unchecked, and more mutations are accumulated over time that extend past the cell cycle to the cellular machinery itself. These mutations, in combination with the genetic mutations accrued through abnormal mitotic progression, eventually cause the cell to be completely deregulated in its growth and proliferation. It becomes unstoppable and even immortal.
  27. MOLECULAR PHARMACOLOGY
  28. Molecular Pharmacology rornmrecabrøb DNAdarnage R*atbnfauts DNAdamage Sphdkdefece GO Growåcondöns fÜs DNAdmage 1. 2. 3. Check points defects as anticancer target: Spindle defects: (by using anti- microtubule drugs) growth conditions: (by using anti proliferative factors e.g. DNA damage, ionizing radiation and UV) Replication faults: (by using anti-metabolites) . Chromosome catenation: (by using topoisomerase inhibitors )
  29. Anti mitotic Agents Antimitotic agents: Anti-tumor agents that inhibit the function of microtubules through the binding of their subunits or through direct cessation of their growth. What are microtubules (MTs)? Protein polymers formed by a-Tubulin and B-tubulin heterodimers that play an important role in critical cell functions such as movement, phagocytosis and axonal transport. They also play a key role in the formation of the mitotic spindle apparatus and cytokinesis at the end of mitosis. • In normal cells, microtubules are formed when a cell starts dividing during mitosis. Once the cell stops dividing, microtubules are broken down or destroyed. The crucial involvement of MTS in mitosis makes them a prime target for anti-cancer agents.
  30. Microtubules growth disassembly Andres M Tubulin dimer protofilament microtubule kinesin dynein
  31. Spindle defects DNA normal metaphase spindle 4 taxol KSP/Eg5 treated spindle nhibited spindle sciencedirect.com vinblastine treated spindle interphase cell after adaptation
  32. Spindle defects Taxol and Its Role in Cancer Treatment
  33. Taxo I Yew tree Small amount in trees (Mostly in bark) Cancer treatment Inhibits cell division and growth
  34. Taxol Affects microtubules Inhibits mitosis Expensive to extract and purify Synthetic synthesis methods Aco o OBz CSA c
  35. P rometa ph ase hase Cytoki 46 t. 92 N and Sep apart diopp.ar c— "gin Two 46 Mitosis and Taxol Spindle assembly Keeps cell in metaphase Cell death Cancer cell growth inhibited
  36. Taxol Prevent the growth of cancer cells by affecting microtubules. • Overall, they encourage microtubule formation, then they stop the microtubules from being broken down so that the cells become so clogged with microtubules that they cannot continue to grow and divide. This results in the cell's arrest in mitosis. • Eventually, cell DEATH by apoptosis.
  37. Complicating Factors B-tubulin mutations which inhibit the binding of taxanes to the correct place on the microtubules; this renders the drug ineffective. • In addition, some resistant cells also display increased aurora kinase, an enzyme that promotes completion of mitosis .
  38. Spindle defects Vinca alkaloids and its role in cancer treatment
  39. Spindle defects Catharanthus roseus is known as the common or Madagascar periwinkle Originally native to island of Madagascar. COPYRIGHT JR MANHARt
  40. Spindle defects OH vincristine CHOOOC CHOO H -%-C2Hs OCOCHz I H *SCOOCH3 CHO HO OH sczHs vinblastine Vincristine and Vinblastine Inhibit mitosis in metaphase by binding tubulin CH300C CH30 &-C2Hs OCOCH3 I H • *COOCH3 CHs HO
  41. Vinca Alkaloids The Vincas work through their ability to bind to the B- tubulin subunit of microtubules, blocking their ability to polymerize with the a- tubulin subunit to form complete microtubules. This causes the cell cycle to arrest in metaphase because, in absence of an intact mitotic spindle, duplicated chromosomes cannot align along the division plate. The ultimate fate of such cells is to undergo apoptosis.
  42. • • Complicating Factors Resistance to the Vinca alkaloids comes in the form of cross- resistance due to the structural similarity of the compounds (multidrug resistance) Because of the heavy concentration of microtubules in the brain and the drug's disruption of this, patients treated with Vinca alkaloids can experience severe neurotoxicity.
  43. Spindle defects Another examples : • • Colchicine :Colchicine is an alkaloid derived from the autumn crocus (Colchicum autumnale). It inhibits mitosis by inhibiting microtubule polymerization. While colchicine is not used to treat cancer in humans, it is commonly used to treat acute attacks of gout . It poison (PMN; Polymorph nuclear Leukocytes ) that mediate joint inflammation . Podophyllotoxin: Podophyllotoxin and Podophyllin, derived from the may apple plant, are used to treat viral skin infections. Griseofulvin: derived from a Penicillium mold, is an antifungal drug.
  44. DISCUSSION
  45. YNVHI
  46. Three apples; Adam's, Newton's, And Steve Jobs

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