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Block 4 Pink sheet answers

by: Bennett Notetaker

Block 4 Pink sheet answers Bio 130, 15017

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Everything you need to know for the last test
BIO130LEC000:Perspectives in Human Bio
James Lafountain
Study Guide
Telomere, Androgen, translocation, fetus
50 ?




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This 4 page Study Guide was uploaded by Bennett Notetaker on Friday April 29, 2016. The Study Guide belongs to Bio 130, 15017 at University at Buffalo taught by James Lafountain in Spring 2016. Since its upload, it has received 49 views.


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Date Created: 04/29/16
1. The function of the G1/S checkpoint is, the cell either enters the next phase of the cycle (S) or it enters a non-dividing state (Go). Many cells stay in the Go until stimulated by external signals to reenter the cycle and divide. The G2 checkpoint is where the cell monitors completion of DNA synthesis and DNA damage, ensures that the DNA has been replicated and that may damage to the DNA which has been repaired. The M checkpoint is when the attachment of the spindle fibers to the chromosomes is monitored. 2. A mitogen is an agent/molecule that stimulates mitosis. The nucleus receives this mitogenic stimulation. Signal transduction is a cellular molecule pathway by which an external signal is converted into a functional response and processes external signals inside of the cell to produce changes in gene expression, leading to cell division. 3. Phosphorylation is a downstream effector it turns on and off by addition or deletion of phosphate ions. ATPADP uses a phosphate to turn it on. Active +inactive+ATPP+ADP (turns it off). 4. Proto-oncogenes are genes that initiate or maintain cell division when the products encoded by these genes are active, cells grow and divide; when they are inactivated, normal cells stop dividing. 5. Ras encodes signal transduction proteins that process growth- promoting signals. Mutant ras protein is active, located on chromosome 5. It’s a proto-oncogene because it normally functions in the regulation of cell cycle progression. The can be inherited or mutation. 6. pRB is the gene product of RB1 gene, which is a tumor suppressor gene. pRB functions in the binding and inactivation of transcription factor of E2F. E2F acts on cell growth-related and division-related genes, when freed E2F activates transcription of genes. pRB binding of E2F suppresses growth and division. A downstream effector is activated. The effector acts on pRB in the nucleus. Mutation of RB1 gene causes loss of control over cell cycle progression and occurs on chromosome 13. Person must be homozygous for the recessive mutant allele. A lot of times one mutant allele is inherited and the other arise spontaneously which is called heteozygosity. 7. Cancer is a genomic disease, from multiple mutations particularly those of proto-oncogenes and tumor-suppressor genes. Multiple mutations are generally regarded to be the basis of a tumor achieving a malignant status capable of exhibiting metastasis. (notion that many different genetic mutations are required for cancer to develop, it explains the progression of cancer) Metastasis is the ability to invade new tissues results from new mutations in cancer cells. Cells detach from the primary tumor and move to other parts of the body, forming new malignant tumors. 8. Cell motility helps with normal development of cells and is a major component of inflammation and wound healing. Consequences of metastasis are painful and untreatable. A person’s physiology is altered. 9. Loss of function is mutant pRB expressed from mutant RB1 oncogene that results in mutant BRCA 1 expressed from mutant BRCA 1 oncogene results in hybrid BCR-ABL protein expressed from Philadelphia chromosome. (causes abnormal white blood cells) 10. Reciprocal translocation is what generates the hybrid BCR- ABL gene on the Philadelphia chromosome. Gleevec is a competitive inhibitor for the ATP binding site on hybrid protein. Philadelphia translocation is spontaneous. 11. Ploidy is a Karyotypic feature determined by the number of sets of chromosomes, which are designated by “n.” For example, haploid- one set (n or 1n) Diploid is 2n triploid is 3n and Tetraploid is 4n. Triploids and greater are called polyploidy. Triploids mostly result from dispermy, fertilization of a normal egg with 2 sperm and are lethal in live births. Tetraploids are found in miscarriages and are a result of normal diploid cell experiencing cytokinesis failure. Aneuploidy is a karyotype having a chromosome number that is not an exact multiple of the haploid set and is usually attributed to genetic non- disjunction a defect in the mechanism of chromosome segregation. Trisomy is Down syndrome, creates behavioral, physical, and mental challenges. 12. Non-disjunction is an outcome of a defective chromosome segregation, at MI secondary spermatocytes or oocytes are (n+1) and (n-1). At MII spermatids or eggs that are (n+1) and (n-1). Non-disjunction may also be an outcome of defective mitosis (2n+1) (2n-1). 13. Trisomy 21 (47,XX,+21) happens 1/800 live birth. Higher than normal susceptibility to infections and other health related conditions, the life expectancy is less than 50yrs. can be either sperm or egg. 14. Klinefelter phenotype has female features, turner syndrome you’ll have lacking functional reproductive tract, Down syndrome has heart defects and physical development is retarded. 15. A baby with Down syndrome (trisomy 21) can have an extra chromosome because of either the sperm or the egg. If the baby were a boy it’s karyotype would be 47,XY+21. Yes sperm can be disomic for chromosome 21. 16. Non-disjunction is an outcome of defective chromosome segregation. During meiosis l, secondary spermatocytes or oocytes are n+1 and n-1. In meiosis ll, spermatids or eggs are n+1 and n-1. Non-disjunction can also be an outcome of defective mitosis, which would be 2n+1, 2n-1. With nondisjunction of defective meiosis correlates with age of maternal germ line. 17. Translocation of a segment chromosome to another chromosome, reciprocal interchange of parts between non- homologous chromosomes. This can be maternal-origin with a non-homologous chromosome of maternal origin. Robertsonian translocation can yield Down syndrome t(14,21), acrocentric chromosomes fuse to form a single centromere. Q arm of chromosome 14 fuses to q arm of chromosome 21. Isochromes have duplication of q arm and loss of p arm, which may create two centromeres. 18. The cytogenetic explanation for monozygotic twins is that the twin with 46,XX has a normal phenotype and the other one does not. Instead, the twin with 45,X karyotypes. 19. The two uncommitted sex duct systems are Mullerian ducts and the Wolffian system. Wolffian survives in males and Mullerian survives in females (the absence of Y allows this). Once the baby is born it is evident because their phenotypes aren’t normal (38 weeks). 20. In order to be fertile a female needs two X chromosomes. When a female karyotype is 45,X they have no ovarian development and their phenotype is immature at puberty and may have infertility. 21. The SRY gene is dependent on the Y chromosome. The gene product is 45, X in 46,XY. This gene encodes a transcription factor. It contains the protein testis-determining factor (TDF), which initiates male sex differentiation. This causes XX male syndrome. Testosterone is a potent androgen secreted by Leydig cells from the developing tests and it develops pre-genitalia and pre-reproductive tract cells of embryonic males. Sertoli cells of the embryonic testes secrete anti-Mullerian hormone. Sertoli cells supply nutrients. Steroid hormones enter through the diffusion across plasma membrane and bind to inactive receptor in the cytosol. Activated receptor and bound hormone diffuse into nucleus. Hormone/receptor complex binds to target genes. 22. AMH is a peptide hormone secreted by Sertoli cells binds to AMH-ll receptors in cell membranes of Mullerian ductwork and initiates a signal cascade, the outcome is a programmed cell death. If androgen hormone receptor is defective or absent in target tissues, then default female development when possessing Y chromosome in males. If it is present then male development occurs. 23. During prophase of meiosis l, replicated homologues pair up to form bivalents. In the normal course of events of meiosis l, there is exchange between homologues. The result is transfer of maternal segments to paternal chromosomes and vise versa. This is similar to translocation but it typically isn’t deleterious. Pairing and exchange between X and Y normally occurs only within the pseudoautosomal segments. XX male syndrome SRY gene on one of the Xs. 46,XY is CAIS female, underdeveloped testes, short vagina, and lacks Mullerian ductwork. 24. Phenotypes: PAIS (46,XY) is underdeveloped male genitalia, underdeveloped testes, some female features. 46,XX, (tx,Y) (+SRY) are male with fully developed male phenotype. 46,XY, (tX,Y) (-SRY) are female. 25. Androgen receptors each consist of a protein that binds the androgen and a portion that binds to DNA in steroid-sensitive areas of nuclear chromatin. Controls transcription of male-related genes. Anti-Mullerian hormone is secreted by the juvenile testes and is present in CAIS female phenotype. 26. Five to six weeks old embryo, eyes, brain, limbs, hand/foot plates are evident but sex differentiation is not evident until eight weeks this is when it becomes a fetus. Male or female phenotype appears at 12 weeks. At 12 weeks a fetus is 2.5 inches long. 27. Telomeres are natural ends located on chromosomes, each has two unless it is replicated then it has four. They are used to protect and stabilize the ends of DNA. Length is maintained by the enzyme telomerase, which is used to replicate the telomeres. Telomerase is found in embryonic cells, germ-line cells, stem cells, and certain cancer cells. In cancer cells, telomerase allows the cell to divide and becomes constitutive element of tumor cells.


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