The Mutation Of Proteins That Affect The Cohesin Pathway

Chromosome pairs line up across the equator of the spindle at metaphase I (5). In anaphase I the chromosomes separate and travel to opposite ends of the spindle. The chromosomes migrate to the equators of two new spindles for metaphase 2 (7). Next the chromatids are pulled apart in anaphase 2 to form four clusters of chromosomes in telophase 2. The nuclear envelopes reform around four haploid nuclei that will give rise gamete

At prophase the chromosomes become condense to become visible and the membrane begins to break down. The chromosomes line up along the centre of the equator during metaphase. The chromatids separate and are pulled to opposite poles during anaphase. In telophase these separate chromatids

The chromosomal abnormalities include turner's disease, laron dwarfism, noonan syndrome, sinotina wiley syndrome, russell xifushi, mutation / deletion of the short stature homeobox-containing gene, and skeletal dysplasia.

Define the term crossing over. (3 points) During meiosis’ prophase the homologous chromatids exchange segments.

A) Meiosis consists of two cell divisions and is broken up into Meiosis I and Meiosis II. At the beginning of the Cell Cycle, in this case there are four chromatids each from the homologous pairs being A, a, B, b. This is the Diploid number (4) meaning it is 2 times the haploid number that will be seen at the end of meiosis II. During the S phase of interphase, the chromatids replicate and reach the end of G2 phase. Now starting meiosis, during the first stage of prophase I the chromosomes condense and pair up through synapsis with their sister chromatids creating AA, aa, BB, bb. After they pair up they go through a process called crossing over, where the homologous chromosomes share a piece of their genetic material with each other. Crossing over allows for the genetic diversity of chromosomes. Now there are four homologous chromosomes Aa, Aa, Bb, Bb, each containing heterozygous alleles because the sister chromatids exchanged genetic information with their homologous pair. During late prophase I, spindle fibers being to form where they will later attach to a homologous chromosomes centromere. The next stage is Metaphase I. During metaphase I, the homologous pairs line up at the metaphase plate, also known to be the center of the cell. The homologous pairs form a tetrad which is considered a group of four homologous chromosomes. These homologous chromosomes orient themselves randomly, which is know as the process of independent

D. The kinetichore is the site of attachment of the centromere to the nuclear spindle apparatus.

Anaphase – the chromosomes are divided into single from pair and the chromosomes move to opposite poles

This syndrome is from a mutation of a gene on chromosome 15 and this causes problems in the production of fibrillin-1 which is a protein that is an important part of connective tissue. The name for the gene is FBN1. Basically, it is the “glue” that helps to support the tissues in the human body. A child born to a parent with this syndrome has a 50% of having it. However, in the remaining 25%, neither parent has the disease which gives them a 1 in 10,000 chance of having a child with this disorder. When a child of two unaffected parents is born with it then the genetic mutation occurs in either the egg or sperm cell at the time of conception.

The phase proceeding metaphase in which chromosomes aligned at the metaphase plate split into two sister chromatids and are pulled to opposite sides of the cell by the mitotic spindle.

Page 20: Sam says, “I’m learning so much, could you tell me the next phase”. Yes, replied the fairy, the next is anaphase during this process the spindles grab the center of the chromosomes called the centromere which binds the two chromatids to form a chromosome. The spindles pull at the chromosomes to the opposite

The main problem with chromosome instability produced by these breaks is the susceptibility to translocations and thus oncogene activation.

This study was performed in order to gain more knowledge on mitosis and meiosis. This lab was done by observing mitosis in plant and animal cells, comparing the relative lengths of the stages of mitosis in onion root tip cells, stimulating the stages of meiosis, observing evidence of crossing-over in meiosis using Sordaria fimicola, and estimating the distance of a gene locus from its centromere. Mitosis is the scientific term for nuclear cell division, where the nucleus of the cell divides, resulting in two sets of identical chromosomes. Mitosis is accompanied by cytokinesis in which the end result is two completely separate cells called daughter cells. There are four phases of mitosis: prophase, metaphase, anaphase and

Error 2: In the video, they state that in anaphase “Each CHROMATID transforms into a CHROMOSOME in its own right…And SPINDLE FIBERS drag them to the POLES.” This is incorrect; the chromatids don’t “transform” into chromosomes. They chromatids pair up to make paired

The proper division of cells is fundamental for growth and reproduction of organisms. Chromosomes must divide evenly and accurately between the two new cells so that harmful mutations are prevented from occurring. Cohesin is an important protein mediator in these precise divisive events. While preparing for mitosis, cohesin forms a ring around DNA to hold sister chromatids together in an organized fashion. Cohesin is comprised of 2 intramolecular coiled coil proteins, Smc1 and Smc3, which dimerize to form a circular protein. The dimerization domain of these proteins, also known as the hinge, keeps these proteins bound together. At the other end of cohesin, the ATPase head domains of Smc1 and Smc3 are held together by Scc1, a kleisin protein essential to the unloading of cohesin during anaphase. Scc1 is cleaved by separase once all chromosomes are attached to microtubules correctly and tension is sensed by the cell. Cleavage of Scc1 allows release of DNA from cohesin and separation of sister chromatids to opposite ends of the cell. The removal of cohesin from DNA is well studied and understood, but there is still controversy regarding the mechanisms of cohesin loading onto DNA.

This tumour is inherited as an autosomal dominant trait as the child inherits one abnormal Rb1 gene, strongly predisposing the child to