A common tactic used to obtain high yields of synchronous developing larvae is to isolate larvae that have advanced Cell Biol. Sepsenwol, S. To prove that the signal results from hybridization of the tagged oligonucleotide to RNA , we treat cells prior to Single- cell Additionally, a novel systems biology tool developed to identify suitable gene targets aimed to optimize and improve Barbosa, T. Differential expression of over 60 chromosomal References AT1 cell - specific markers are expressed by AEC with time in culture , suggesting an active transition An improved method for isolating type II cells in high yield and purity.
Antalis , T. Skip to content. The book reviews key cell biology concepts needed to study molecular biology, and reviews the key concepts of molecular biology necessary for clinical medical practice, Flow charts provide a clear overview of molecular biology techniques and how they are applied in medicine. A chapter on understanding the research literature provides a solid background in molecular biology protocol so that students can understand the purpose and thinking behind published research articles.
Numerous illustrations and tables supplement the text. Need-to-know information is presented in a clear, concise outline format. Additional features include updated drug references, a drug index, key points in bold, and tables summarizing key facts. Whether a student is reviewing for the end-of-year exams in pharmacology or brushing up for the USMLE, this book provides a quick overview of this challenging topic. Highlights of this edition include a brief glossary of key neuroanatomical structures and disease states; addition of an icon to more clearly identify the Clinical Correlations sections; an appendicized table of common neurological lesions; expanded figure legends that identify clinically relevant anatomical relationships; an improved, expanded index; and modified text and figure legends to comply with Terminologia Anatomica.
The information found in this text provides a comprehensive overview of physiology in a concentrated format and serves as a valuable resource for course and board review. The book is generously illustrated with schematic line drawings as well as photographs of the most clinically relevant diseases.
Illustrations appear at the end of each chapter in a multi-panel figure, similar to a mini-atlas. The most important information is presented in an uncluttered outline format, with numerous line drawings and tables, NB Nota Bene boxes highlighting pathology pearls, and hundreds of review questions.
This edition has been fully updated and includes a new High-Yield Glossary of Terms at the end of the book. BRS Genetics addresses a field that is increasingly taught in shorter courses. Coding regions exons; "expression sequences" make up a minority of the nucleotide sequences of a gene. Histone proteins are small and contain a high proportion of lysine and arginine amino acids.
Lysine and arginine give the proteins a positive charge that enhances binding to negatively charged DNA. H1 histone protein joins nucleosomes to form a nm fiber. Types of chromatin. Heterochromatin and euchromatin active and inactive are packed in the cell nucleus. Ten percent of the chromatin is highly condensed, transcriptionally inactive heterochromatin.
Ninety percent of the chromatin is less condensed: ten percent is transcriptionally active euchromatin and eighty percent is transcriptionally inactive euchromatin. Degree of compaction 1. Human chromosome 1 contains approximately ,, base pairs.
The distance between each base pair is 0. The DNA in chromosome I is 88,, nm, or 88, f.. Lm long ,, x 0. During metaphase, the chromosomes condense, and the 88, f.. Lm of DNA is reduced to 10 f..
Lm, an fold compaction Figure Figure Chemical structure of the components of DNA purines, pyrimidines, sugars, and phosphate , which form a polynucleotide chain. Note the phosphodiester bond. H3,H4 30 nm fiber Extended chromatin Secondary loops and extended chromatin Condensed mitotic chromosome Figure Levels of packaging of double-helix deoxyribonucleic acid DNA within a chromoso me during metaphase.
Histone Hl joins the nucleosomes to form a 30 nm diameter fiber that consists of either extended chromati n or secondary loops within a condensed mitotic chromoso me. New York, Garland Publishing, , p C DNA synthesis on the lagging strand proceeds differently than on the leading strand. Okazaki fragments end when they join a downstream RNA primer. Finally, DNA ligase joins the Okazaki fragments.
DNA ligase joins the repeats to the lagging strand. A nucleas e cleaves the ends to form double-helix DNA with flush ends. Depuri nation 1. Each J ay, the DNA of each human cell loses approximately purines A or G when the N-glycosyl bond betwee n the purine and the deoxyribose sugar phosph ate is broken.
Depuri nation is the most commo n type of damage to DNA. When it occurs, the deoxyribose sugar phosph ate is missing a purine base.
To begin repair, AP apurinic site endonu clease recognizes the site of the missing purine and nicks the deoxyribose sugar phosph ate. A phosph odieste rase excises the deoxyribose sugar phosph ate. Deamin ation of cytosin e C to uracil U 1. Each day, approximately cytosines spontaneously deamin ate to uracil. If the uracil is not restored to cytosine, then at replication, an incorre ct U-A base pairing occurs instead of a correct C-G base pairing. To begin repair, the enzyme uracil- DNA glycosidase recognizes and removes uracil.
It does not remove thymin e because thymin e is distinguished from uracil by a methyl group on carbon 5. An AP apyriminic site endonu clease recognizes the site of the missing base and nicks the deoxyribose sugar phosph ate. Pyrimid ine dimeriz ation 1. Sunligh t [ultraviolet UV radiation] causes covalen t linkage of adjacen t pyrimidines, forming, for example, thymin e dimers. To begin repair, the uvrABC enzyme recognizes the pyrimidine dimer and excises a residue oligonucleotide that includes the dimer.
Xerode rma pigmen tosum XP 1. XP causes hypersensitivity to sunligh t UV radiatio n and, as a result, severe skin lesions and skin cancer. Most patients die before they are 30 years old. XP is probably caused by an inability to remove pyrimidine dimers, most likely because of a genetic defect in one or more enzymes involved in their removaL In humans, removal of these dimers requires at least eight gene products.
Ataxia-telangiectasia 1. Ataxia-telangiectasia causes hypersensitivity to ionizing radiation and, as a result, cerebellar ataxia, oculocutaneous telangiectasia, and immunodeficiency.
Ataxia-telangiectasia is probably caused by defects in the enzymes involved in DNA repair. Fanconi's anemia 1. Fanconi's anemia causes hypersensitivity to DNA cross-linking agents and, as a result, leukemia and progressive aplastic anemia. Fanconi's anemia is probably caused by defects in the enzymes involved in DNA repair. Bloom syndrome 1. Bloom syndrome causes hypersensitivity to many DNA-damaging agents and, as a result, immunodeficiency, growth retardation, and predisposition to cancer.
Bloom syndrome is probably caused by widespread defects in the enzymes involved in DNA repair. Early diagnosis improves survival because the early stage of HNPCC is the outgrowth of small benign polyps that are easily removed.
Althou gh DNA replicat ion and repair is crucial to cell surviva l, it does not explain human genetic variability. Some of the variability is imported by DNA rearran gement s that are caused by genetic recomb ination , either general or site-specific.
An importa nt example of general recomb ination occurs during "crossi ng over," when two homolo gous chromosomes pair during meiosis gamete formati on. During synapsis, RecA protein allows the single strand to invade and interact with the double- h elix DNA of the other chromosome. This interact ion requires DNA sequenc e h omology.
A DNA strand on the homologous chromosome repeats this process to form an important interme diate structur e crosso ver exchan ge, or Hollida y junctio n that has two crossing strands and two noncrossing strands. Many DNA viruses and other transposable elemen ts see Chapte r 4 encode for a recom- bination enzyme called integra se or transpo sase, respectively. DNA repair occurs to fill the gaps. The two types of genetic recombination.
A General recombination during meiosis. B Sitespecific recombination during deoxyribonucleic acid DNA viral infection. Transposable elements are mobile deoxyribonucleic acid DNA sequences that jump from one place in the genome to another transpos ition. The cause of transposition is unclear. Nine percent of the human gen ome consists of two families of transposable elements: 1. Transposable elements undergo long quiescent periods followed by periods of intense movement transposition bursts.
These bursts contribute to the genetic variability of the genome. Transposase is a recombin ation enzyme similar to integrase. It cuts the rransposable element at sites marked by inverted repeat DNA sequence s that are approximately 20 base pairs long. Transposase is encoded in the DNA of the transposable element.
The transposable element is inserted at a new location, possibly on another chromosome. The transposable element undergoes transcription, which produces an RNA copy that encodes a reverse transcriptase enzyme. The transposable element is inserted at a new location by a mechanis m similar to the one that an RNA virus retroviru s uses to transform h ost DNA. Mechanisms of transposition. A Transpositi on as double-stranded deoxyribon ucleic acid DNA.
B Transposition through a ribonucleic acid RNA intermediate. Transposable element s affect the genetic variability of an organism in several ways: A.
After transposase removes the transposable element from its site on the host chro- mosome , the host DNA undergoes DNA repair. A mutatio n may occur at the repair site.
If the transposable element moves to the target DNA near an active gene, the transposable element may affect the level of gene expression. Most of these changes in the level of gene expression would be detrimen tal to the organism. However, over time, some changes might be beneficial and spread through the populati on. If the transposable element moves to the target DNA in the center of a gene sequenc e, the gene is mutated and inactiva ted.
Gene transfer see Figure D 1. If two transpos able element s are close together, the transpos ition mechani sm may cut the ends of both of them. The DNA between the two transposable element s will move to a new location. If the DNA contains a gene, the gene is transferred to a new location.
Gene transfer is especially importa nt in the develop ment of antibioti c resistan ce in bacteria. For example, if the bacteria l DNA between the two transposable element s contains the gene for tetracyc line resistance, then the recipien t bacteriu m becomes resistant to tetracycl ine. Effect of transposable elements on genetic variability.
A Mutation at the former site of the transposable element TE. B Effect on the level of gene expression. C Gene inactivati on. D Gene transfer. Decreased gene. Gene amplification occurs when repeated rounds of deoxyribonucleic acid DNA synthesis yield multiple copies of a gene. The copies are arranged as tandem arrays within a chromosome.
Gene amplification usually results in increased levels of the protein that the gene encodes. Drug resistance in cancer cells. Cancer cells may become resistant to methotrexate , a B. Methotrexate inhibits dihydrofolate reductase, which is involved in DNA synthesis. Cancer cells often become resistant to methotrexate through amplification of the dihydrofolate reductase gene.
This amplification increases dihydrofolate reductase levels, which overcome effective inhibition by methotrexa[e. Amplification of genes involved in the cell cycle proto,oncog enes. Proto,oncoge ne amplification contributes to uncontrolled cell growth and tumor development. See Chapter Gene Amplification j Figure Gene amplification. Laboratory procedures to manipulate deoxyribonuc leic acid DNA [recombinan t DNA technology] drove many important discoveries that affect clinical medicine.
Understandin g these discoveries requires an unJerstandin g of DNA laboratory procedures. These enzymes are crucial to DNA technology because treating a specific DNA sample with a particular restriction enzyme always produces the same pattern of DNA fragments.
After a DNA sample is fragmented with a restriction enzyme, the fragments are separated by size with gel electrophoresis. The sizes of the DNA fragments are compared, and a physical restriction map of the sample is constructed to show each cut site. Restriction maps provide useful information about a DNA sample, but the ultimate physical map of DNA is its nucleotide sequence, which is established with DNA sequencing.
This method combines DNA synthesis with dideoxyribon ucleoside triphosphates that lack the 3'-0H group that they normally contain. If a dideoxyribonucleoside triphosphate is incorporated into DNA during DNA synthesis, addition of the next nucleotide is blocked hecause the 3 '-OH group is missing. This blocking is the basis for the enzymatic method of DNA sequencing.
A DNA probe is a single-stranded DNA segment an oligonucleoti de with base pairs that participates in a hybridization reaction.
In a hybridization reaction, a single-strand ed DNA segment e. This reaction exploits a fundamental property of DNA to denature and renature. Action of restriction enzymes.
The specific nucleotide sequences recognized by each restriction enzyme and the cut sites A Y are shown. Alui produces DNA fragments that have blunt ends. B A long DNA sequence h as many cut sites. If the same sequence is treated with both EcoRI and Alul, the same four DNA fragmen ts are always produced because the restriction enzymes are specific.
P renatal testing for sickle cell anemia see Figure B. Gene cloning and sequencing permits the creation of a DNA probe that hybridizes with the gene e.
Sickle cell anemia is a recessive genetic disease that is caused by a mutation in the p-globin gene. This mutation converts a single amino acid in the p-globin protein from glutamic acid normal to valine mutant. Because both the normal gene and the mutant gene have been sequenced, DNA probes can locate both genes with Southern blotting.
The mixture of DNA fragments obtained from this treatment is placed at the top of an agarose gel slab. Under an electric field, the DNA fragments move through the gel toward the positive electrode because DNA is negatively charged. DNA fragments in the mixture are separated by size. Small DNA fragments migrate faster than large fragments. Therefore, small fragments are located at the bottom of the gel, and large fragments are located at the top.
To permit visualization of the DNA fragments, the gel is soaked in a dye that binds to DNA and fluoresces under ultraviolet light. New York, Garland Puhlishing, , p. Prenatal testing for other genetic diseases. Several single-gene disorders are diagnosed prenatally with DNA analysis, including the following: 1. Autosomal dominant disorders a. Huntington's disease b. Myo tonic dystrophy C. Here on stuvera. High School Biology Book provides the basics and fundamentals needs for an easy Biology Have you been However to read campbell College Botany Volume 1 pdf Free Download With easy digital access to pdf and eBooks , learning is at your fingertips.
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