Introductory Remarks
Dongyou Liu in Handbook of Tumor Syndromes, 2020
Structurally, each chromosome consists of two sister chromatids (or two identical chromosome copies) that are connected (aligned) in the centromeric region (or centromere), giving the appearance of an X (or H), and separating each chromatid (chromosome copy) into a short (p) arm and a long (q) arm, which together form about 400 total bands in a karyotype using Giemsa stain. At the ends of linear chromatids (chromosome copies) are telomeres (repetitive stretches of DNA) that lose a bit of the DNA with each cell division. A cell dies when all of the telomere DNA is lost [5]. However, some malignant cells manage to acquire the ability to keep their telomeres intact during division, and thus facilitate their continued/uncontrolled growth. Further, heterozygous germline mutation refers to change in a gene on one chromatid in germ cells (egg or sperm), which is inherited from a parent; homozygous germline mutations refer to similar changes in a gene on both chromatids in germ cells, which are inherited from two carrier parents; and compound heterozygous germline mutations refer to distinct changes in a gene involving both chromatids in germ cells, which are inherited from two carrier parents.
B Cells and Humoral Immunity
Constantin A. Bona, Francisco A. Bonilla in Textbook of Immunology, 2019
Two additional mechanisms may also result in class-switching, although they are not thought to occur with significant frequency, if at all. One hypothesis is identical to the differential splicing of a transcript containing μ and δ. If we imagine that RNA polymerase may continue along the DNA transcribing all of the C region genes, then VDJH joined to any isotype can be generated by differential splicing. Another model for class-switching invokes unequal sister chromatid exchange. During mitosis, sister chromatids may exchange some portions of themselves. If the positions of the joints between chromatids are identical, one has homologous recombination, or equal crossing over. The amount of genetic information in each chromatid remains unchanged. If the breaks occur in different positions in the chromatids, one has non-homologous recombination, or unequal crossing over. This results in deletion of genetic information from one chromatid, and its duplication in the other.
Polar body biopsy and its clinical application
David K. Gardner, Ariel Weissman, Colin M. Howles, Zeev Shoham in Textbook of Assisted Reproductive Techniques, 2017
During the first meiotic division, the diploid chromosome content of an oocyte is reduced to two haploid chromosome sets, which both consist of paired chromatids. One paired chromatid set is extruded as part of the first PB. Sperm entry into an oocyte initiates the second meiotic division, whereby the set of paired chromatids is separated and a single chromatid set becomes part of the second PB. After the first meiotic division, the number of the chromosomes in the oocyte and the first PB should be identical and the same holds true for the number of chromatids following the second meiotic division. Numerical chromosomal abnormalities can be caused by non-disjunction, meaning that a whole chromosome is not directed to the proper compartment (either the oocyte or PB). Another mechanism is premature chromatid segregation into two single, separated chromatids, which has been suggested to occur frequently prior to the first meiotic division (27) and has been confirmed by clinical data (19). Premature chromatid segregation during meiosis I can either lead to a balanced situation, where both chromatids remain in the same compartment, or to an unbalanced situation, where the two chromatids are finally allocated to different compartments. Some of the unbalanced segregations that originate in meiosis I in the oocyte can be corrected in meiosis II during formation of the second PB (28), and can even give rise to a normal child (21).
Cadmium exposure and DNA damage (genotoxicity): a systematic review and meta-analysis
Published in Critical Reviews in Toxicology, 2022
Raju Nagaraju, Ravibabu Kalahasthi, Rakesh Balachandar, Bhavani Shankara Bagepally
The frequency of SCE and chromosomal aberrations (CAs) in peripheral blood lymphocytes are extensively studied to screen genotoxicity in occupational settings (Roussel et al. 2019; Meyer et al. 2020). In this SRMA, three studies have used SCE to predict genotoxicity in the Cd-exposed group. SCE represents physical exchanges of the parental strands in the duplicated chromosomes during replication. Therefore, it is used as a genetic indicator for potential genotoxins/mutagens, as most forms of DNA damage induce chromatid exchange upon replication fork collapse (Wilson and Thompson 2007). SCE is a more sensitive biomarker for genotoxic effects than structural aberrations (Tucker and Preston 1996). In the present SRMA, the frequency of SCEs is elevated among the Cd-exposed than the unexposed group. The findings show the possibility of DNA damage among the Cd-exposed group.
Targeting the DNA damage response in pediatric malignancies
Published in Expert Review of Anticancer Therapy, 2022
Jenna M Gedminas, Theodore W Laetsch
Double stranded DNA breaks can be repaired using nonhomologous end joining repair (NHEJ) or homologous recombination (HR). The repair mechanism used is based on the stability of the end of the DNA breaks [11]. NHEJ directly ligates broken DNA without the need for a homologous template [12]. Because it does not rely on a template, it is able to repair double stranded breaks in any phase of the cell cycle, however, it is also more prone to error than homologous recombination. Homologous recombination is responsible for the reactivation of stalled replication forks and repair of double stranded DNA breaks and inter-strand crosslinks [13]. The repair process occurs in three steps. The broken end of the chromosome if first paired with the homologous region on the sister chromatid. That strand is then invaded to form a Holliday junction, or DNA crossover, which generates a DNA duplex from the two different chromatids [14]. The Holliday junction is then translocated along the DNA and eventually cleaved by endonucleases to again form separate DNA molecules [14]. These two processes are activated by several kinase pathways, ataxia telangiectasia mutated (ATM), ataxia telangiectasia related (ATR), and DNA-PK, which when mutated, result in defective double-strand break repair [15].
Chromosome aberration in typical biological systems under exposure to low- and high-intensity magnetic fields
Published in Electromagnetic Biology and Medicine, 2020
Emanuele Calabrò, Hit Kishore Goswami, Salvatore Magazù
It is known that the most crucial stage of mitotic division is the interphase wherein each very long chromatin thread (actually, chromatid) becomes a chromosome by way of replication of DNA and the immediate influence becomes operative of coiling and condensation so as to result in making compact chromosome. This packaging of DNA by tortuously folding and compacting into shaping a thick rod-shaped chromosome with two chromatids continues until early metaphase. It is precisely at this stage that alignment of chromosomes along the direction of the applied magnetic field was observed after exposure, such as it appears in Figures 7c–d and 9b. These changes have been the most common and repeated results observed in root tip preparations of both garlic and broad bean.
Related Knowledge Centers
- Anaphase
- Centromere
- DNA
- Homologous Chromosome
- Ploidy
- Sexual Reproduction
- Sister Chromatids
- Zygosity
- Meiosis
- Chromosome
- DNA