Health | Learn about Genetic Mutations. Health | Learn about Genetics. March CFA by Pearson Prentice Hall. February CFA by Pearson Prentice Hall. January CFA by Pearson Prentice Hall. Fires. Dept of Molecular and Cellular Biology, Harvard U: Biology Links. Genetic Origins. DNALC Kits. * BioServers. GeneBoy - DNALC Bioinformatics 2003. Silencing Genomes. Cancer Biology – Inside Cancer: A Multimedia Guide to Cancer. 06 Lecture Animation Ppt. 09 Lecture Animation Ppt. 10 Lecture Animation Ppt. Central Dogma Of Dna. Gene therapy. Cloning. Journey of Man: A Genetic Odyssey. DNA Structure - Contents page.
An Interactive Animated Nonlinear Tutorial by Eric MartzAdapted for using Jmol instead of Chime, by Angel Herráez Part of Biomodel website by Angel Herráez, Univ. de Alcalá (Spain) Disponible también en español. Também disponível em português. Auch verfügbar auf Deutsch. Disponible aussi en français. This version 4.3 works in any Java-compatible browser. If you prefer using Chime for molecular models, the page using it is still available, with equivalent content and functionality. This tutorial is designed to complement Biology or Biochemistry and Molecular Biology books, so it is not by itself a complete introduction to DNA structure. Before proceeding, check that your browser has Java installed and can use the Jmol software: This tutorial is designed to complement an introduction to DNA, by providing tools for a self-directed exploration.
Methods, Acknowledgements, and References. Do you know there are more tutorials at MolviZ.Org? More about Jmol: Jmol home page. Version history. DNA From The Beginning. ΕΚΠΑΙΔΕΥΣΗ ΜΕΣΑ ΑΠΟ ΤΗΝ ΒΙΟΛΟΓΙΑ. Home of CELLS alive! Mental Health. Cells. Learn.Genetics™ Cellular Aging: Telomeres - Telomeres Are Chromosome Caps, Telomere Structure, Telomeres And Replication, Telomeres And Replicative Senescence, Telomeres And Premature Aging Syndromes.
Aging is a complex process that occurs on multiple levels. The end result of aging is that life span is limited in multicellular organisms. The cells that make up multicellular organisms also have limited life spans. The limitation on cellular life span is comprised of two parts: (1) cells become unable to continue dividing but remain metabolically active, and (2) at some future time cell death occurs. Many cells in the human body are continually undergoing cellular division. Cellular division is a normal condition of certain tissues; examples include hair growth, the sloughing off of skin every several days, and the complete turnover and replacement of the cells of the immune systems every few months. In the 1960s, Leonard Hayflick first noted that human cells undergo a limited number of divisions when placed in culture.
Junk DNA - Junk DNA & Evolution. The most interesting genetic homologies are in junk DNA. Often called "noncoding DNA," junk DNA has no apparent function or produce no protein but may help regulate the gene. When DNA is transcribed, pieces either do not get transcribed at all or are only partially transcribed, with no functional protein produced. You can cut out or modify most junk DNA without affecting the organism.
There are several varieties of junk DNA including pseudogenes, introns, transposons and retroposons. Is Junk DNA Useless? Stretches of non-coding DNA were originally labelled "Junk DNA" on the assumption that non-coding sequences did nothing at all. Our knowledge of how DNA works has vastly improved, though, and this is no longer the accepted position among biologists. The function of over 95 percent of our DNA is still a mystery. Bryan D. Importance of Junk DNA Why is junk DNA so interesting? The same can be said of DNA. Junk DNA Homologies. ATP and Energy Storage. Organize-It: Test Yourself on Biology Categories. Biology in Motion. Cancer Cells in Culture. Aging. What is Aging? Aging is the progressive loss of physiological functions that increases the probability of death.
This table gives some data. The decline in function certainly occurs within cells. This is especially true of cells that are no longer in the cell cycle: neurons in the brain; skeletal and cardiac muscle; kidney cells. Tissue and organs made of cells that are replenished by mitosis throughout life. e.g., blood intestinal epithelium show far fewer signs of aging. In the natural world, very few animals live long enough to show signs of aging. Random mortality from starvation predation infectious disease a harsh environment (e.g., cold) kills off most animals long before they begin to show signs of aging. Even for humans, aging has only become common in recent decades. At the start of the 20th century, infectious diseases such as pneumonia and influenza caused more deaths in the United States than "organic" diseases like cancer.
Aging in Invertebrates Aging in Vertebrates Why Do We Age? Telomeres. Each eukaryotic chromosome consists of a single molecule of DNA associated with a variety of proteins. The DNA molecules in eukaryotic chromosomes are linear; i.e., have two ends. (This is in contrast to such bacterial chromosomes as that in E. coli that is a closed circle, i.e. has no ends.) The DNA molecule of a typical chromosome contains a linear array of genes (encoding proteins and RNAs) interspersed with much noncoding DNA.
Included in the noncoding DNA are long stretches that make up the centromere and long stretches at the ends of the chromosome, the telomeres. Telomeres are crucial to the life of the cell. They keep the ends of the various chromosomes in the cell from accidentally becoming attached to each other. The telomeres of humans consist of as many as 2000 repeats of the sequence 5' GGTTAG 3'. Replication of linear chromosomes presents a special problem. DNA polymerase can only synthesize a new strand of DNA as it moves along the template strand in the 3' –> 5' direction.
Orbital tumors: diagnosis and treatment. DNA trick throws ageing into reverse - health - 29 November 2010. A technique to keep the tips of your chromosomes healthy could reverse tissue ageing. The work, which was done in mice, is yet more evidence of a causal link between chromosome length and age-related disease. Telomeres, the caps of DNA which protect the ends of chromosomes, shorten every time cells divide. But cells stop dividing and die when telomeres drop below a certain length – a normal part of ageing. The enzyme telomerase slows this degradation by adding new DNA to the ends of telomeres.
Mariela Jaskelioff and her colleagues at the Dana Farber Cancer Institute in Boston, Massachusetts, engineered mice with short telomeres and inactive telomerase to see what would happen when they turned the enzyme back on. Four weeks after the team switched on the enzyme, they found that tissue had regenerated in several organs, new brain cells were developing and the mice were living longer. Journal reference: Nature, DOI: 10.1038/nature09603 New Scientist Not just a website! More From New Scientist. Mitosis. Mitosis, reproducción celular. Mitosis.