what are the kinds of chromosomal aberation?
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Chromosomal aberrations include\n1) inversions (rearrangements of DNA segments within chromosomes)\n2) reciprocal translocations (DNA segments exchanged between chromosomes)\n3) aneuploidies (deviations from the normal diploid number of chromosomes in somatic cells, either because different chromosomes join, or there is one or more extra chromosomes, etc.)\n4) transpositions (a chromosome segment is transfered to another place in the same or a different chromosome).
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We normally have 23 pairs of chromosomes, that is, 46 chromosomes in total. When they're seen inside of a cell nucleus, they just look like similar V , X and Y shaped little dark spots, but the specialists are able to order them and know which ones belong to each pair (i.e. are homologous). They've labeled the pairs from 1 to 23 (the 23rd pair is the XX or XY sex chromosomes). \nIn Down syndrome, there is an extra chromosome. If you just looked at an image of the nucleus, you'd just count 47 chromosomes. But it has been determined that the "extra" one is a duplicate of one of the members of pair 21. \nIn the case of other duplicate chromosomes, the effects are not Down syndrome. Most cases of chromosomal duplication are lethal.
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the chromosomes group together.
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Caused by a terminal deletion of the most distal band of the short arm of chromosome 1, monosomy 1p36 is the most commonly observed terminal chromosomal deletion, occurring in approximately 1 in 5,000 births (Shaffer and Lupski 2000; Heilstedt et al. 2003b). As first described by the Shaffer lab in 13 subjects (Shapira et al. 1997), craniofacial characteristics of this contiguous gene deletion syndrome (CGDS)--so-called because it involves the deletion of multiple adjacent genes on the same chromosome arm--include late-closing, large anterior fontanels (membranous intervals at the intersection of the cranial bones at the crown of the skull), brachycephaly (disproportionate shortness of the head), deep-set eyes, flat nasal bridge, asymmetric ears, and pointed chin. Monosomy 1p36 is also associated with mental retardation, developmental delay, hearing impairment, seizures, growth impairment, and heart defects (Shapira et al. 1997; Slavotinek et al. 1999; Heilstedt et al. 2003a). Over 90 subjects with rearrangements of 1p36 have enrolled in our studies, of which 61 were recently published (Heilstedt et al. 2003a). The deletion sizes in the subjects vary considerably (Wu et al. 1999; Heilstedt et al. 2003a); however, there is some uniformity in the origin of the deletions, with over 60% being maternally derived (Wu et al. 1999; Heilstedt et al. 2003a). Candidate genes have been proposed for some of the individual features of monosomy 1p36, including seizures (Heilstedt et al. 2001) and facial clefting anomalies (Colmenares et al. 2002). \n\nThe Shaffer laboratory has recently identified possible mechanisms for the generation and/or stabilization of terminal deletions of 1p (Ballif et al. 2003; Ballif et al. 2004a; Ballif et al. 2004b; Gajecka et al. 2005). In addition, the Shaffer laboratory has recently demonstrated the use of microarrays--a rapid, sensitive, and high-resolution technology for the detection of many chromosomal anomalies--in the detection of deletions of 1p36 (Yu et al. 2003). \n\n\ncheck this article\n\nShapira SK, McCaskill C, Northrup H, Spikes AS, Elder FF, Sutton VR, Korenberg JR, Greenberg F, Shaffer LG (1997) Chromosome 1p36 deletions: the clinical phenotype and molecular characterization of a common newly delineated syndrome. Am J Hum Genet 61:642-650
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Submetacentric chromosomes have a centromere that is off-center, so that one chromosome arm is longer than the other. When chromosomes are aligned, they are oriented so that the short arm, designated "p" is at the top, and the long arm, designated "q" (simply for what follows the letter "p"), is at the bottom.
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There are very many.  Sickle cell anemia, for example, is caused by an inherited mutation in the gene for one of the subunits of hemoglobin, the oxygen-carrying protein in blood.   Certain types of cancer no doubt result from mutations in critical parts of the genome -- either induced by carcinogens or radiation, or just bad luck.  Besides mutation, there are a litany of other genetic abnormalities which can cause disease.  Huntington's disease, for example, is caused by having too many repeats of a certain DNA fragment.  Down's syndrome is caused by having an entire extra chromosome.  As you can see, DNA is the cause of many diseases, and it will be the target of many future cures as we get better at molecular therapy.
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Realistically, none, because the chromosomes will cross over during meiosis, so none of the chromsomes will be exactly as they descended from the parents.\n\nBut if the haploid number is 6, and you pretend there's no crossing over, then there are 2^6 ways for the chromosomes to assort, and 2 of them will be 6 chromosomes from a single parent.  So that's 1 in 32, or about 3%.
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Hi.  I found a link to which will help you answering your question.\n\nThis is not my field of expertise, but I'm guessing the darker sections indicate heterochoramtin.  This is the portion of the chromosome that not currently being used for expression of proteins.\n\nHope this helps.  Pass on the good karma!
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Let's assume you want a human example.\nHuman cells have 46 chromosomes.\n\nIn Meiosis 1:\nProphase 1- chromosomes replicate, join with homologous pairs to become tetrads.\n--46 chromosomes paired, 23 tetrads, and 92 chromatids\nMetaphase 1- same numbers as prophase\nAnaphase 1: 46 chromosomes (double stranded), 92 chromatids\nTelophase 1: end: 23 chromosomes (double stranded), 46 chromatids per cell\n\nProphase 2: same as Telophase 1\nMetaphase 2: same as Telophase 1\nAnaphase 2: 46 chromosomes, zero chromatids\nTelophase 2: end: 23 chromosomes per cell.
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diploidization\n\ndoubling of chromosome no.\nthis method is usually implied in plants to double their chromosomal configuration
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Either a trisomy or a monosomy.  A trisomy is when you have an extra copy of a chromosome, and a monosomy is when you're missing one.  Down's syndrom is one example of a trisomy (specifically trisomy 22), but there are others.  Most are lethal for embryos, but children with some other trisomies can survive.
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one chromosome comes from each parent
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Interphase\n\nhttp://www.cellsalive.com/cell_cycle.htm
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During Meiosis I the chromosomes engage in crossing over through their association with homologs.\n\nMy bad. Tetrads is what the four chromosome arrangement is called.\n\nYes the site is a chiasma.
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a chromatid forms one part of a chromosome after it has coalesced for the process of mitosis or meiosis. during either process, the word "chromosome" indicates a pair of two exactly identical or "sister" chromatids joined at the central point of each chromatid, called the centromere.\n\na chromosome, by definition, has exactly one centromere. thus when sister chromatids are pulled apart by the mitotic spindle during anaphase - that is, when the centromere joining two sister chromatids splits into two centromeres - then each sister chromatid becomes an independent chromosome.\n\nin non-gametic, non-dividing human cells, there are 23 pairs of chromosomes and thus 46 chromatids.
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if you mean Y Chromosome...then check out this website:\n\nhttp://en.wikipedia.org/wiki/Y_chromosome\n\nThe Y chromosome is "shorter" then the X chromosome.\n\nAlso:\nThere has been higher insidence of a smaller Y choromosome with trisomy 21 (Down Syndrome).
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none\n\n\nyou start with one pair of homologous chromosomes in prophase I of meiosis I.  at metaphase I, these homologues line up across the metaphase plate, and at anaphase, they seperate so that one homologue goes to one pole, and the other homologue goes to the other pole.  after cytokinesis at the end of telophase I, you have one homologue in each cell...that homologue then goes through meiosis II, and at metaphase II, that homologue lines up at the metaphase plate with each sister chromatid facing each pole, and the chromosome is "pulled apart".  Anaphase II pulls the sister chromatids to each pole, and cytokinesis splits the one cell into two....two cells, each containing one sister chromatid of a homologous pair. (although in some text books this is refered to as a single homologue)