Properties of Satellite Chromosomes

Properties of Satellite Chromosomes

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I have some questions regarding Satellite chromsomes which could not be resolved by a google search.

  1. Does the satellite consist of telomeric sequences ?

  2. If not, What is the function of a satellite ? And where will the telomeric sequences be present - in the main body ? On the secondary constriction ?

  3. Satellite chromosomes are also known as SAT chromosome which stands for Sino Acid Thymidine. I read in some sources that SAT means without thymidine. But how is that possible, if there is A then obviously there has to be T ? ( in dsDNA)

If by "satellite chromosomes" you mean "satellite repeats", then:

  1. Not always. There many types of satellites, such as telomeric, centromeric (like gamma, alpha, beta satellites), simple repeats (CT)n.
  2. It is still an open question. Some say they are important for chromosome structure (e.g., centromeres). Sometimes satellites get transcribed as might act as lncRNAs. And of course, most of them are just junk DNA.
  3. If there isTthen there isAtoo.


  1. Satellites contain telomeric repeats at their ends as all chromosomes do. But they are more about NOR repeats.

  2. They are important for the nucleolus functioning. But shorts arms of acrocentric chromosomes are not crucial, take Robertsonian translocation as an example.

DNA, which constitutes the genome of a cell, is always packaged with a variety of proteins, and together these make up the chromosomes. A chromosome serves to compact the DNA and protect it from the damage, while at the same time allowing the genes it contains to be available for transcription into RNA. In addition to these functions, extra ones are necessary when the cell divides. Prior to cell division the DNA must be copied and these copies separated (segregated) and delivered to different parts of the cell, ensuring that each of the new cells receives only a single copy.

To ensure correct segregation, chromosomes have to have distinct components that are composed of specific DNA sequences and associated proteins. Bacterial chromosomes, (plasmids ) which are circular, have a single site at which DNA replication originates, and attachment to the cell membrane results in segregation. Artificial bacterial chromosomes (BACs) mimic this using appropriate origin sequences.

In organisms with multiple linear chromosomes (eukaryotic organisms) the process is more complicated. The ends of the chromosomes must be protected from degradation and from the mechanisms that the cell uses to protect itself against broken DNA. Telomeres , which provide these functions, are arrays of short, repeated sequences with complexes of specific proteins attached. To ensure segregation complexes of other proteins, DNA sequences known as kinetochores form at sites known as centromeres . These contain molecular motors, systems to monitor correct segregation, and sites for attachment of microtubules . Chromosomes will contain one or more origins of replication.

Chromosome Structure

With different phases of cell cycle the changes of chromosome structure takes place. At the time of interphase, the chromosomes remain in the form of network fine thread, namely chromatin threads. But during metaphase and Anaphase, the contract and shorten to form distinct rod-like structures. Distinct arm-like chromatid formed of coiled chromonema and knob like protein particles called chromomeres are showed by them. A primary constriction which is known as centromere and a secondary constriction present in some chromosomes, which is associated with nucleolus formation and for this reason it is called nucleolus organiser. A part of chromatid may be depressed off from the secondary constriction which is known as satellite devoid by nucleic acid.

The study of chromosome structure is mainly done from the root tip or the shoot tip of plants which contains the Meristematic tissue or from the pollen mother cells of plants and tissue from sex glands and W.B.C. in animals.
Some chromosome structures we may define under: –

i) Primary or centromeric constriction : the non-stained notched region of a chromosome containing centromere is known as primary or Centromeric constriction.
It appears as a gap in the chromosome, but originally there is no shortage of chromatin here. It is invisible due to its property of non-staining. They contain the centromere, which is variable in position and imparts various shapes to the chromosomes at the time of the anaphasic separation.
ii) Centromere: The centromere is the spherical chromomeric structure at the centre of the primary constriction responsible for the attachment of the chromosome to the spindle fibre. Normally majority of chromosomes have one centromere sometimes chromosomes may break to form acntric fragments which are lost during cell division. In the chromosome structure the centromere is the point where the two arms of chromosome meet it determines the shape of the chromosome. The microtubules of the spindle gets attached to the centromere and the anaphasic separation of the chromosome is initiated.

Classification of chromosome on the basis of centromeric position: -

a) Metacentric: - In this case the centromere occurs at the centre of the chromosome which dvides the chromosome into two equal arms.
b) Sub-metacentric: - In such case the centremereoccursvery close to the centre of the chromosome dividing it into two equal arms.
c) Acrocentric: - Here the centromere occur very close to the terminal end of the chromosome forming one very long and one very short arm.
d) Telocentric: - In this case the centromere is almost terminally situated on a chromosome.
iii) Kinetochore: - The protein disc attached to the centromeric chromomeres to which the spindle microtubules are joined these are called the kinetochore of chromosome structure. They bind with the microtubule of the spindle fibre.
iv) Secondary Constriction: - Any constriction other than the primary constriction is termed as secondary constriction. They help in the organization of the nucleolus and synthesize m-RNA.

v) Chromatid and Chromonema: It is one of the identical strands of chromosome developing during its replication. At their early stage of condensation the chromatids is called chromonema.
The chromonema is the site where DNA remains in pack.
vi) Chromomere: The chromomere are stainable bead-like structures arranged along the chromosome. In the early prophase of mitosis and meiosis the chromomeres are present. In the chromosome structure they appear as beaded necklace, where the bead like chromomeres are attached to interchromomeric thread. The chromomere are the structural component of chromosome but do not actually represent the genes.
vii) Telomeres: The telomeres are the terminal end of chromosomes. They are formed of heterochromatin and contain repetitive DNA, remains associated with nuclear envelope. The telomeres impart polarity to chromosomes and prevent joining of the chromosome fragments and associated with the production of enzyme telomerease.
viii) Satellite: The satellite is the terminal round knob-like heterochromatin body beyond the secondary constriction of a chromosome. The shape and size of it is constant in a chromosome and its diameter is same as the chromatid. By a thin chromatin filament the satellite is connected to the chromatid. There is no specific function of a satellite but it is just a morphological feature of chromosome structure.


To examine the chromatin composition of human artificial chromosomes, we used a panel of artificial chromosomes formed after transfection with vectors containing either synthetic chromosome 17 (D17Z1) or cloned X chromosome (DXZ1) alpha-satellite sequences [12, 14]. Each of the artificial chromosomes tested contains a functional de novo centromere assembled from the transfected DNA, as well as at least one copy of a functioning gene used as a selectable marker. Together, this panel of artificial chromosomes provides an opportunity to examine the nature of heterochromatin and euchromatin assembled on the transfected DNA sequences. The high mitotic stability and de novo composition of artificial chromosomes generated from D17Z1 (17-E29, 17-D34 and 17-B12) or DXZ1 (X-4 and X-5) have been described [12, 14]. As a more direct measure of artificial chromosome segregation errors, we have used an assay that allows cells to undergo anaphase but cannot complete cytokinesis [14]. Using fluorescence in situ hybridization (FISH), artificial and host chromosome segregation products can be measured and nondisjunction or anaphase lag defects recorded.

In X-4 and X-5, artificial chromosomes mis-segregated in 1.8% and 2.4% of cells, respectively ([14] and Table 1). Similar analyses of artificial chromosome segregation errors in 17-B12 revealed that they mis-segregated in 2.4% of the cells (Table 1). This segregation error rate is comparable to that found for the majority of other human artificial chromosomes previously characterized [14]. Artificial chromosomes in 17-E29 and 17-D34 have segregation efficiencies corresponding to more than 99.9% per cell division, using metaphase analyses [12]. For comparison, we also examined an additional cell line, 17-C20, which contains highly mitotically unstable D17Z1-based artificial chromosomes. In 17-C20, artificial chromosome copy number was high (average 4.7 per cell) and artificial chromosomes were lost from the cell population by 30-40 days of culture without selection, despite containing both inner (CENP-A) and outer (CENP-E) kinetochore proteins (data not shown). In the anaphase assay, 12.2% of artificial chromosomes in 17-C20 were mis-segregating (at 12 days without selection) and the predominant defect was anaphase lag (Table 1). Sizes of D17Z1-containing artificial chromosomes were based on comparison of the signal intensity on the approximately 3 Mb D17Z1 array on chromosome 17 to intensities on the artificial chromosomes using FISH analyses with a D17Z1 probe (Table 2 see also Figures 2 and 3 in [12]). Artificial chromosomes that had signal intensities several-fold less than the endogenous D17Z1 signals were estimated to be 1-3 Mb in size, whereas artificial chromosomes that produced signals similar to or several-fold more intense than those of the endogenous D17Z1 arrays were estimated to be in the 3-10 Mb size range. Similar comparisons of the signal intensities on the DXZ1-based artificial chromosomes with those of the host DXZ1 signals were used to estimate the sizes of the DXZ1-based human artificial chromosomes (Table 2 and data not shown). Properties of artificial chromosomes used in the present study are summarized in Tables 1 and 2.

Variation in levels of heterochromatin-associated factors correlates with artificial chromosome size

To test whether human artificial chromosomes were capable of forming heterochromatin, we first examined several established markers of heterochromatin on the artificial chromosome panel. Indirect immunofluorescence with an antibody recognizing histone H3 modified by trimethylation at lysine 9 and lysine 27 (H3TrimK9/K27) was applied to metaphase spreads. Methylation of lysines at these sites has been associated with formation of repressive chromatin, including pericentric heterochromatin in mouse cells [32, 51–53, 59, 60]. As shown in Figure 1a and 1b, small D17Z1-based artificial chromosomes, estimated to be in the 1-3 Mb size range (Table 2), do not stain detectably with the H3TrimK9/K27 antibody, in contrast to the centromeric regions of the natural human chromosomes that stain, in some cases intensely, with this antibody. On the other hand, larger artificial chromosomes, estimated to be in the 3-20 Mb size range (Table 2), stained strongly for H3TrimK9/K27 modifications (Figure 1c-g), often at levels greater than those of many endogenous centromeric regions (Figure 1g). It is clear that at least large amounts of transfected alpha satellite are capable of assembling into heterochromatin in the context of human artificial chromosomes. Whether small artificial chromosomes are truly negative for this marker of heterochromatin, or whether they assemble only small amounts of heterochromatin below the level of detection, cannot be assessed with this assay. Nonetheless, they clearly have assembled far less of this epigenetically modified heterochromatin than exists at the relevant endogenous 17 centromeric regions (Figure 1).

Heterochromatin forms on artificial chromosomes in the 3-20 Mb size range but is depleted on smaller artificial chromosomes that are approximately 1-3 Mb. Indirect immunofluorescence using an antibody that recognizes modification of histone H3 by trimethylation at lysine 9/lysine 27 (H3TrimK9/K27) (red signal) demonstrated that these heterochromatin markers are not detectable on the smaller D17Z1-based artificial chromosomes (arrowheads) in lines (a) 17-D34 and (b) 17-E29, but are readily detectable on the larger D17Z1- and DXZ1-based artificial chromosomes (arrowheads) as shown in lines (c) 17-B12, (d) 17-C20, (e) X-4 and (f) X-5. Arrows indicate chromosome 17 centromere regions (a-d) or host X centromere regions (e, f). Host D17Z1 sequences typically stained positive for H3TrimK9/K27 in most spreads (arrows in a-d). It was difficult to detect the X centromere signal (for example, arrow in (e)) but in about 30% of spreads there was a clearly positive signal as indicated by the arrow in (f). (g) Variation in H3TrimK9/K27 levels at host centromere regions is shown in a larger area of the spread shown in (c): artificial chromosomes are indicated by arrowheads arrows point to the consistently strongly positive signals on the long arm of the Y chromosome (Yq). Artificial chromosome size estimates are listed in Table 2. Confirmation of artificial chromosomes and relevant host centromere regions were determined by FISH analyses with appropriate alpha-satellite probes (data not shown).

In a parallel approach, we examined the distribution of HP1α in four lines containing D17Z1-based artificial chromosomes. Each line was stably transfected with a Myc-epitope tagged form of HP1α (see Materials and methods) to permit detection of HP1α using an anti-Myc antibody. The smaller artificial chromosomes stained very weakly (at a level similar to that of the staining on the euchromatic chromosome arms), well below the levels of HP1α detected at the centromeric region of the endogenous chromosome 17s (Figure 2a,b). As seen with the H3TrimK9/K27 antibody, the larger artificial chromosomes stained strongly for HP1α (Figure 2c,d), at levels comparable to the endogenous chromosome 17s. The intensity of HP1α-Myc staining was variable at endogenous human centromere regions (Figure 2d) similar results were obtained using a primary anti-HP1α antibody (data not shown). This contrasts with the amount of CENP-A, which appears to be present at consistent levels at all normal human centromeres [61] and artificial chromosomes tested (Figure 2d) [12, 13, 58]. Notably, the CENP-A signal is localized to a discrete subdomain within the larger artificial chromosomes, whereas HP1α covers a much larger area of the artificial chromosome (Figure 2d). This suggests that HP1α may be a marker for generalized pericentromeric heterochromatin that flanks the kinetochore-associated alpha satellite of the functional centromere, rather than a marker of the functional centromere per se. Such a model [2, 3] is also consistent with the observation that small artificial chromosomes, which contain little if any of the flanking heterochromatin, do not contain elevated levels of HP1α (Figure 2a,b Table 2).

Detection of HP1α on D17Z1-based artificial chromosomes. (a-d) Cell lines stably expressing a Myc-tagged form of HP1α. HP1α was detected using an anti-Myc antibody (red). The artificial chromosomes (about 1-3 Mb indicated by small arrows) in lines (a) 17-D34-1.A2 and (b) 17-E29-1.C23 exhibit faint HP1α staining at a level similar to the general arm staining. Larger artificial chromosomes (3-10 Mb small arrow) in lines (c) 17-C20-1.B22 and (d) 17-B12-1.B10 stain strongly for HP1α. Inserts in (a-c) show either DAPI (blue)-stained artificial chromosomes or HP1α (red). Host 17 centromere regions are indicated by the large arrows in (a-c). In (d), simultaneous staining for CENP-A (green) shows that CENP-A is restricted to a portion of the artificial chromosome (arrows) whereas the HP1α signal coats the entire artificial chromosome. In contrast to CENP-A, which is present at comparable levels on all artificial chromosomes tested [12,13,58] and host kinetochores [61], HP1α staining levels are more variable at host centromere regions (d).

Euchromatin forms on artificial chromosomes

For their potential use as gene-transfer vectors or as general vehicles suitable for interrogation of genome function, human artificial chromosomes must also be capable of forming euchromatin to support gene expression. Indeed, one would hypothesize that at least small amounts of transcriptionally active chromatin must form during artificial chromosome formation to permit expression of the selectable marker gene(s) contained on the transfected constructs [10, 12, 14]. It has previously been shown using immunocytochemical methods [62, 63] that methylation of histone H3 at lysine 4, an epigenetic modification associated with transcriptionally permissive chromatin [64–66], is generally enriched on autosomes and depleted at the repressed inactive X chromosome and human centromere regions.

As a test for formation of permissive chromatin on artificial chromosomes, we stained metaphase spreads with an antibody that recognizes histone H3 dimethylated at lysine 4 (H3DimK4). All artificial chromosomes tested stained positively for H3DimK4 modifications (Figure 3a-f Table 2). In contrast, the endogenous centromeric regions were depleted for H3DimK4 staining, although, as noted above for markers of heterochromatin formation, this depletion may reflect the state of the surrounding heterochromatin, rather than that of the functional centromere per se.

Transcriptionally competent chromatin is present on artificial chromosomes. Dimethylation of lysine 4 on histone H3 (H3DimK4) was visualized using an antibody against H3DimK4 (red). This euchromatin mark was detected on all artificial chromosomes (arrowheads) generated from either D17Z1 in lines (a) 17-D34, (b) 17-E29, (c) 17-B12 and (d) 17-C20, or DXZ1 in lines (e) X-4 or (f) X-5. Host centromere regions were generally depleted for H3DimK4 as indicated by arrows pointing to centromere regions of chromosome 17 (a-d) and the X chromosome (e, f).

Previous structural analyses of artificial chromosomes indicate that they consist of input DNA multimers arranged as blocks of alpha-satellite DNA interspersed with vector sequences [7, 11, 12]. This structural organization is consistent with the presence of multiple selectable marker genes and differs from the large uninterrupted blocks of alpha-satellite DNA found at all human centromeres that are typically under-represented for this active chromatin mark (Figure 3). Because mitotically stable artificial chromosomes can have permissive as well as repressive chromatin present, these data suggest that this chromatin configuration does not significantly disturb mitotic centromere function.

Two modes of artificial chromosome replication timing

While the genomic determinants of potential origins of DNA replication in the human genome, as well as of their timing of replication during S phase, are still not well understood, the generally accepted paradigm is that expressed sequences replicate in the first half of S phase, while non-expressed sequences replicate in the second half [67]. Consistent with this pattern, alpha-satellite DNA, as well as constitutive heterochromatin (such as that found on the Yq arm), replicate in the mid to late S phase period [54, 55, 68, 69]. In the present study, we have asked whether D17Z1-based artificial chromosomes replicate at a similar time to endogenous chromosome 17 alpha-satellite DNA. To determine the time of replication, unsynchronized cells were pulsed with bromodeoxyuridine (BrdU) for 2 hours, followed by a thymidine chase for varying lengths of time before harvesting cells in metaphase (see Materials and methods). Detection of BrdU incorporation at sites of DNA replication was performed using indirect immunofluorescence with an anti-BrdU antibody on metaphase spreads.

While there was overlap between artificial chromosome replication timing patterns and those of the host 17 centromere regions during mid S phase (Table 3), we found two modes of artificial chromosome replication timing. The heterochromatin-enriched artificial chromosomes (17-B12 and 17-C20 see Table 2) commenced replication in mid S phase (2-4 hours into S phase) and completed replication by 6 hours into S phase (Figures 4 and 5c Table 3). In contrast, the heterochromatin-depleted artificial chromosomes (17-D34 and 17-E29 see Table 2) started replicating within the first 2 hours of S phase (early S phase) and their replication was completed by 4 hours into S phase (Figure 5a,b Table 3). That these differences are characteristic of each particular artificial chromosome is suggested by the observation that, in all lines, when multiple artificial chromosomes were present in a given cell, they are frequently replicated synchronously (Figures 4c and 5a,c). From these data, it is tempting to propose that the presence of large amounts of heterochomatin in the larger artificial chromosomes may have influenced replication timing on these artificial chromosomes and promoted a shift towards later in S phase.

Replication timing of human artificial chromosomes in line 17-B12. BrdU detection (red) in cells that have been blocked with colcemid in mitosis following BrdU pulses during S phase (see Materials and methods). Artificial chromosome (small arrows enlarged artificial chromosomes are shown in inserts) and chromosome 17 (large arrow) locations in each spread were confirmed by FISH analyses using a D17Z1 probe (data not shown). (a-d) Images from different periods in S phase. (a) Early in S phase, at 0-2 h, the two artificial chromosomes present in this spread are not replicating. Some incorporation of BrdU on chromosome 17 is detectable. (b) In the middle of S phase, at 2-4 h, two of four artificial chromosomes are replicating. (c) Later, at 4-6 h, all three artificial chromosomes are being coordinately replicated. Some BrdU incorporation within chromosome 17 arms is detectable. (d) Late in S phase, at 6-8 h, artificial chromosomes are not replicating. The centromere region on chromosome 17 is replicating (large arrow). Because of the A-rich sequence composition of satellite III on Yq, BrdU is preferentially incorporated into one strand, producing an asymmetrical staining pattern on Yq (arrowheads) [84].

Replication timing in different human artificial chromosomes. (a-c) Detection of BrdU (red) on artificial chromosomes (small arrows larger version in inserts). (a) In mid S phase, at 2-4 h, two artificial chromosomes in line 17-D34 are BrdU positive. (b) The artificial chromosome in line 17-E29 is replicating early in S phase, in the 0-2 h period. (c) In mid S phase (2-4 h), three artificial chromosomes are being coordinately replicated in this spread from line 17-C20. Images shown are from the first half of S phase, and, as expected, Yq (arrowhead) is not replicating at this time.

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It has recently been suggested that observed levels of variation at microsatellite loci can be used to infer patterns of selection in genomes and to assess demographic history. In order to evaluate the feasibility of these suggestions it is necessary to know something about how levels of variation at microsatellite loci are expected to fluctuate due simply to stochasticity in the processes of mutation and inheritance (genetic sampling). Here we use recently derived properties of the stepwise mutation model to place confidence intervals around the variance in repeat score that is expected at mutation-drift equilibrium and outline a statistical test for whether an observed value differs significantly from expectation. We also develop confidence intervals for the time course of the buildup of variation following a complete elimination of variation, such as might be caused by a selective sweep or an extreme population bottleneck. We apply these methods to the variation observed at human Y-specific microsatellites. Although a number of authors have suggested the possibility of a very recent sweep, our analyses suggest that a sweep or extreme bottleneck is unlikely to have occurred anytime during the last approximately 74,000 years. To generate this result we use a recently estimated mutation rate for microsatellite loci of 5.6 x 10(-4) along with the variation observed at autosomal microsatellite loci to estimate the human effective population size. This estimate is 18,000, implying an effective number of 4,500 Y chromosomes. One important general conclusion to emerge from this study is that in order to reject mutation-drift equilibrium at a set of linked microsatellite loci it is necessary to have an unreasonably large number of loci unless the observed variance is far below that expected at mutation-drift equilibrium.

Status of the current preliminary genome assemblies

Preliminary assemblies for alligator and crocodile are available. The assembly for alligator additionally uses information from a 120× physical coverage, Illumina 1.5 kbp mate-pair library. The current crocodile assembly was generated with 80× coverage from a 380 bp paired-end Illumina library. The statistics for the length and contiguity of these two assemblies are shown in Table 1. These assembly statistics are on par with other early stage de novo assemblies using short read data [7, 70].

To obtain early estimates of potential TE content, we analyzed the current assemblies using RepeatMasker and a custom repeat library. The library consisted of all vertebrate TEs identified in RepBase [71] and a set of potential TEs identified by applying RepeatScout [72] to both raw 454 data and to the current assemblies (D. Ray, unpublished data). Consistent with earlier studies [59, 73, 74], much of the repetitive content of the genome comprises non-long terminal repeat (non-LTR) retrotransposons from the CR1 family (Figure 3). There is also high content of Chompy-like miniature inverted-repeat transposable elements (MITEs) [75], Penelope retrotransposons, ancient short interspersed repetitive elements (SINEs), and satellite/low complexity regions. Overall, 23.44% of the alligator and 27.22% of the crocodile genome assemblies are annotated as repetitive compared with 50.63% seen in humans. Thus, this preliminary analysis provides further evidence that these reptilian genomes might be easier to assemble than typical mammalian genomes due to their lower repeat content.

The size of different repeat families classified in our current alligator and crocodile assemblies. Despite more long-distance insert libraries for alligator, more repeats were found in the crocodile assembly. This strongly suggests that crocodiles have more repeats than do alligators, and perhaps the difference will become even more striking as the crocodile assembly improves.

We also examined GC content across the assemblies (Figure 4). Alligators and crocodiles appear to have a higher mean GC content than many other vertebrates. Additionally their large standard deviation in GC content across contigs is similar to that of birds and mammals, suggesting that their base composition is heterogeneous and likely contains GC-rich isochores. This is unlike the situation in the lizard (Anolis) and frog (Xenopus), which lack strong isochores based upon analyses of genomic data [76], or the turtle Trachemys scripta, which appears to lack strong isochores based upon analyses of expressed genes [77]. However, these results are consistent with previous analyses of ESTs that suggested the existence of GC-rich isochores in the alligator genome [62, 77]. Thus, these crocodilian genome data extend the results of the previous analyses and confirm the genome-wide nature of GC-content heterogeneity in crocodilian. We expect improved crocodilian genome assemblies to further illuminate the details of isochore structure in reptiles.

The distribution of GC proportion across several species. Note that alligators and crocodiles have a higher overall proportion of GC than many other vertebrates, as predicted by early BAC-end scans [42]. Abbreviation: SD standard deviation.


We have presented the hypothesis that pericentromeric satellite DNA mediates chromocenter formation, which functions to encapsulate the full set of chromosomes into a single nucleus. Given the ubiquity of satellite DNA, we postulate that chromocenter formation and function may be a universal mechanism conserved across many species.

This hypothesis leads to a few speculations that may provide further insights into the biology of chromocenter. First, in certain cases, eukaryotic chromosomes appear to be completely lacking satellite DNA (e.g., horse chromosome 11, orangutan chromosome 12) (Wade et al. 2009 Piras et al. 2010 Locke et al. 2011) raising the question of if/how these chromosomes may be incorporated into chromocenters. Interestingly, a recent report has shown that transposable element (TE)-derived tandem repeats are a component of mouse chromocenters (Kuznetsova et al. 2016). TE-derived sequences are abundant, heterochromatinized and typically interspersed throughout eukaryotic chromosomes (Saksouk et al. 2015 Nishibuchi and Déjardin 2017), including pericentromeric heterochromatin, where they are present in complex islands within large satellite DNA tracts (Sun et al. 1997, 2003). In addition, satellite DNA is derived from transposable elements in certain cases (Heikkinen et al. 1995 Kapitonov et al. 1998 Kidwell 2002). Recognition of TE-derived repeats or their heterochromatic nature may help chromocenter formation, possibly mediating incorporation of satellite DNA-free chromosomes into chromocenters. Thus, chromosomes lacking typical satellite DNA might still participate in chromocenter formation via their resident TEs. Also, if TE-derived sequences indeed function to mediate chromocenter formation, it may force us to reconsider the biological status of TEs: instead of pure parasites, they may be symbionts of eukaryotic genomes.

The hypothesis that pericentromeric satellite DNA may be a critical component of chromosomes to ensure its maintenance leads to another interesting consideration. Generally, repetitive sequences are thought to be inherently unstable because of sporadic loss of copy number caused by intrachromatid recombination (Charlesworth et al. 1994 Stephan and Cho 1994). If satellite DNA were a critical structural component of the chromosome, it would have to be actively maintained. This is consistent with the fact that satellite DNA shows little within-species variation in the genomes of Drosophila species despite its potential instability (Bosco et al. 2007). Strikingly, it has been shown that satellite DNA can expand in cancer cells (Bersani et al. 2015). Although it was regarded as an “abnormality” of cancer cells, it might reflect the acquired immortality of cancer cells. Similar to the telomere maintenance mechanism, which is confined to immortal cells (germ cells, some somatic stem cells, and cancer cells), maintenance (expansion) of satellite DNA may be a privileged process that can only occur in immortal cells.

Which X Chromosome Becomes the Barr Body?

It is totally random which chromosome becomes inactivated, but within any particular cell, the inactivated X chromosome remains inactive for the cell’s whole life. Furthermore, the same chromosome will be inactive in all the cells that descend from the original one, and, needless to say, the same applies to the active X chromosome. Therefore, there’s only ever one active X chromosome in any given cell, but it varies which X chromosome it is. For that reason, the number of Barr bodies is always one less than the total number of X chromosomes. This is true even when an individual has a mutation that has led to the presence of extra X chromosomes, as in the case of Klinefelter syndrome in males, where an extra X chromosome is found in all cells.

B chromosomes: from cytogenetics to systems biology

Though hundreds to thousands of reports have described the distribution of B chromosomes among diverse eukaryote groups, a comprehensive theory of their biological role has not yet clearly emerged. B chromosomes are classically understood as a sea of repetitive DNA sequences that are poor in genes and are maintained by a parasitic-drive mechanism during cell division. Recent developments in high-throughput DNA/RNA analyses have increased the resolution of B chromosome biology beyond those of classical and molecular cytogenetic methods B chromosomes contain many transcriptionally active sequences, including genes, and can modulate the activity of autosomal genes. Furthermore, the most recent knowledge obtained from omics analyses, which is associated with a systemic view, has demonstrated that B chromosomes can influence cell biology in a complex way, possibly favoring their own maintenance and perpetuation.

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Watch the video: What Can The Most Powerful Satellites Really Do? (July 2022).


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