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Journal articles on the topic 'Packing chromatic number'

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Published: 7 July 2024

Last updated: 7 July 2024

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1

Brešar, Boštjan, Sandi Klavžar, Douglas F. Rall, and Kirsti Wash. "Packing chromatic number versus chromatic and clique number." Aequationes mathematicae 92, no. 3 (December 13, 2017): 497–513. http://dx.doi.org/10.1007/s00010-017-0520-9.

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2

Durgun, Derya, and Busra Ozen-Dortok. "Packing chromatic number of transformation graphs." Thermal Science 23, Suppl. 6 (2019): 1991–95. http://dx.doi.org/10.2298/tsci190720363d.

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Graph coloring is an assignment of labels called colors to elements of a graph. The packing coloring was introduced by Goddard et al. [1] in 2008 which is a kind of coloring of a graph. This problem is NP-complete for general graphs. In this paper, we consider some transformation graphs and generalized their packing chromatic numbers.

3

Balogh, József, Alexandr Kostochka, and Xujun Liu. "Packing chromatic number of cubic graphs." Discrete Mathematics 341, no. 2 (February 2018): 474–83. http://dx.doi.org/10.1016/j.disc.2017.09.014.

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4

Ekstein, Jan, Přemysl Holub, and Bernard Lidický. "Packing chromatic number of distance graphs." Discrete Applied Mathematics 160, no. 4-5 (March 2012): 518–24. http://dx.doi.org/10.1016/j.dam.2011.11.022.

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5

Torres, Pablo, and Mario Valencia-Pabon. "The packing chromatic number of hypercubes." Discrete Applied Mathematics 190-191 (August 2015): 127–40. http://dx.doi.org/10.1016/j.dam.2015.04.006.

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6

William, Albert, Roy Santiago, and Indra Rajasingh. "Packing Chromatic Number of Cycle Related Graphs." International Journal of Mathematics and Soft Computing 4, no. 1 (January 1, 2014): 27. http://dx.doi.org/10.26708/ijmsc.2014.1.4.04.

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7

Torres, Pablo, and Mario Valencia-Pabon. "On the packing chromatic number of hypercubes." Electronic Notes in Discrete Mathematics 44 (November 2013): 263–68. http://dx.doi.org/10.1016/j.endm.2013.10.041.

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8

Ferme, Jasmina. "A characterization of 4-χρ-(vertex-)critical graphs." Filomat 36, no. 19 (2022): 6481–501. http://dx.doi.org/10.2298/fil2219481f.

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Given a graph G, a function c : V(G) ?{1,..., k} with the property that for every u?v, c(u) = c(v) = i implies that the distance between u and v is greater than i, is called a k-packing coloring of G. The smallest integer k for which there exists a k-packing coloring of G is called the packing chromatic number of G, and is denoted by ??(G). Packing chromatic vertex-critical graphs are the graphs G for which ??(G ? x) < ??(G) holds for every vertex x of G. A graph G is called a packing chromatic critical graph if for every proper subgraph H of G, ??(H) < ??(G). Both of the mentioned variations of critical graphs with respect to the packing chromatic number have already been studied [6, 23]. All packing chromatic (vertex-)critical graphs G with ??(G) = 3 were characterized, while there were known only partial results for graphs G with ??(G) = 4. In this paper, we provide characterizations of all packing chromatic vertex-critical graphs G with ??(G) = 4 and all packing chromatic critical graphs G with ??(G) = 4.

9

Lemdani, Rachid, Moncef Abbas, and Jasmina Ferme. "Packing chromatic numbers of finite super subdivisions of graphs." Filomat 34, no. 10 (2020): 3275–86. http://dx.doi.org/10.2298/fil2010275l.

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Given a graph G and a positive integer i, an i-packing in G is a subset W of the vertex set of G such that the distance between any two distinct vertices from W is greater than i. The packing chromatic number of a graph G, ??(G), is the smallest integer k such that the vertex set of G can be partitioned into sets Vi, i ? {1,..., k}, where each Vi is an i-packing. In this paper, we present some general properties of packing chromatic numbers of finite super subdivisions of graphs. We determine the packing chromatic numbers of the finite super subdivisions of complete graphs, cycles and some neighborhood corona graphs.

10

CHALUVARAJU, B., and M. KUMARA. "The Packing Chromatic Number of Different Jump Sizes of Circulant Graphs." Journal of Ultra Scientist of Physical Sciences Section A 33, no. 5 (August 23, 2021): 66–73. http://dx.doi.org/10.22147/jusps-a/330501.

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The packing chromatic number χ_{p}(G) of a graph G = (V,E) is the smallest integer k such that the vertex set V(G) can be partitioned into disjoint classes V1 ,V2 ,...,Vk , where vertices in Vi have pairwise distance greater than i. In this paper, we compute the packing chromatic number of circulant graphs with different jump sizes._{}

11

Goddard, Wayne, and Honghai Xu. "The S-packing chromatic number of a graph." Discussiones Mathematicae Graph Theory 32, no. 4 (2012): 795. http://dx.doi.org/10.7151/dmgt.1642.

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12

Brešar, Boštjan, Sandi Klavžar, and Douglas F. Rall. "Packing Chromatic Number of Base-3 Sierpiński Graphs." Graphs and Combinatorics 32, no. 4 (November 14, 2015): 1313–27. http://dx.doi.org/10.1007/s00373-015-1647-x.

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13

Balogh, József, Alexandr Kostochka, and Xujun Liu. "Packing Chromatic Number of Subdivisions of Cubic Graphs." Graphs and Combinatorics 35, no. 2 (February 2, 2019): 513–37. http://dx.doi.org/10.1007/s00373-019-02016-3.

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14

Finbow, Arthur S., and Douglas F. Rall. "On the packing chromatic number of some lattices." Discrete Applied Mathematics 158, no. 12 (June 2010): 1224–28. http://dx.doi.org/10.1016/j.dam.2009.06.001.

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15

Fiala, Jiří, Sandi Klavžar, and Bernard Lidický. "The packing chromatic number of infinite product graphs." European Journal of Combinatorics 30, no. 5 (July 2009): 1101–13. http://dx.doi.org/10.1016/j.ejc.2008.09.014.

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16

Fresán-Figueroa, J., D. González-Moreno, and M. Olsen. "On the packing chromatic number of Moore graphs." Discrete Applied Mathematics 289 (January 2021): 185–93. http://dx.doi.org/10.1016/j.dam.2020.10.009.

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17

Gastineau, Nicolas, Hamamache Kheddouci, and Olivier Togni. "Subdivision into i-packings and S-packing chromatic number of some lattices." Ars Mathematica Contemporanea 9, no. 2 (August 7, 2015): 321–44. http://dx.doi.org/10.26493/1855-3974.436.178.

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18

Brešar, Boštjan, Sandi Klavžar, Douglas F. Rall, and Kirsti Wash. "Packing chromatic number under local changes in a graph." Discrete Mathematics 340, no. 5 (May 2017): 1110–15. http://dx.doi.org/10.1016/j.disc.2016.09.030.

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19

Gastineau, Nicolas, Přemysl Holub, and Olivier Togni. "On the packing chromatic number of subcubic outerplanar graphs." Discrete Applied Mathematics 255 (February 2019): 209–21. http://dx.doi.org/10.1016/j.dam.2018.07.034.

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20

Božović, Dragana, and Iztok Peterin. "A note on the packing chromatic number of lexicographic products." Discrete Applied Mathematics 293 (April 2021): 34–37. http://dx.doi.org/10.1016/j.dam.2021.01.010.

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21

William, Albert, S. Roy, and Indra Rajasingh. "Packing Chromatic Number of Circular Fans and Mesh of Trees." International Journal of Mathematics and Soft Computing 4, no. 2 (July 13, 2014): 145. http://dx.doi.org/10.26708/ijmsc.2014.2.4.15.

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22

Korže, Danilo, and Aleksander Vesel. "On the packing chromatic number of square and hexagonal lattice." Ars Mathematica Contemporanea 7, no. 1 (January 7, 2013): 13–22. http://dx.doi.org/10.26493/1855-3974.255.88d.

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23

Roy, S. "Packing chromatic number of certain fan and wheel related graphs." AKCE International Journal of Graphs and Combinatorics 14, no. 1 (April 1, 2017): 63–69. http://dx.doi.org/10.1016/j.akcej.2016.11.001.

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24

Urenda, Alje Marie M., Jacel Angeline V. Lingcong, Normina A. Batucan, Joel G. Adanza, and Michael P. Baldado Jr. "Packing chromatic number of the join of some classes of graphs." International Mathematical Forum 17, no. 2 (2022): 75–87. http://dx.doi.org/10.12988/imf.2022.912315.

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25

Brešar, Boštjan, and Jasmina Ferme. "An infinite family of subcubic graphs with unbounded packing chromatic number." Discrete Mathematics 341, no. 8 (August 2018): 2337–42. http://dx.doi.org/10.1016/j.disc.2018.05.004.

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26

Bidine, Ez-Zobair, Taoufiq Gadi, and Mustapha Kchikech. "The exponential growth of the packing chromatic number of iterated Mycielskians." Discrete Applied Mathematics 341 (December 2023): 232–41. http://dx.doi.org/10.1016/j.dam.2023.08.007.

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27

Brešar, Boštjan, Sandi Klavžar, and Douglas F. Rall. "On the packing chromatic number of Cartesian products, hexagonal lattice, and trees." Discrete Applied Mathematics 155, no. 17 (October 2007): 2303–11. http://dx.doi.org/10.1016/j.dam.2007.06.008.

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28

Brešar, Boštjan, Sandi Klavžar, and Douglas F. Rall. "On the packing chromatic number of Cartesian products, hexagonal lattice, and trees." Electronic Notes in Discrete Mathematics 29 (August 2007): 237–41. http://dx.doi.org/10.1016/j.endm.2007.07.040.

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29

Ferme, Jasmina, and Dasa Stesl. "On distance dominator packing coloring in graphs." Filomat 35, no. 12 (2021): 4005–16. http://dx.doi.org/10.2298/fil2112005f.

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Let G be a graph and let S = (s1,s2,..., sk) be a non-decreasing sequence of positive integers. An S-packing coloring of G is a mapping c : V(G) ? {1, 2,..., k} with the following property: if c(u) = c(v) = i, then d(u,v) > si for any i ? {1, 2,...,k}. In particular, if S = (1, 2, 3, ..., k), then S-packing coloring of G is well known under the name packing coloring. Next, let r be a positive integer and u,v ? V(G). A vertex u r-distance dominates a vertex v if dG(u, v)? r. In this paper, we present a new concept of a coloring, namely distance dominator packing coloring, defined as follows. A coloring c is a distance dominator packing coloring of G if it is a packing coloring of G and for each x ? V(G) there exists i ? {1,2, 3,...} such that x i-distance dominates each vertex from the color class of color i. The smallest integer k such that there exists a distance dominator packing coloring of G using k colors, is the distance dominator packing chromatic number of G, denoted by ?d?(G). In this paper, we provide some lower and upper bounds on the distance dominator packing chromatic number, characterize graphs G with ?d?(G) ? {2,3}, and provide the exact values of ?d?(G) when G is a complete graph, a star, a wheel, a cycle or a path. In addition, we consider the relation between ?? (G) and ?d?(G) for a graph G.

30

Citra, S. M., A. I. Kristiana, R. Adawiyah, Dafik, and R. M. Prihandini. "On the packing chromatic number of vertex amalgamation of some related tree graph." Journal of Physics: Conference Series 1836, no. 1 (March 1, 2021): 012025. http://dx.doi.org/10.1088/1742-6596/1836/1/012025.

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31

Rall, Douglas F., Boštjan Brešar, Arthur S. Finbow, and Sandi Klavžar. "On the Packing Chromatic Number of Trees, Cartesian Products and Some Infinite Graphs." Electronic Notes in Discrete Mathematics 30 (February 2008): 57–61. http://dx.doi.org/10.1016/j.endm.2008.01.011.

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32

Martin, Barnaby, Franco Raimondi, Taolue Chen, and Jos Martin. "The packing chromatic number of the infinite square lattice is between 13 and 15." Discrete Applied Mathematics 225 (July 2017): 136–42. http://dx.doi.org/10.1016/j.dam.2017.03.013.

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33

BUJTÁS, CSILLA, GYÖRGY DÓSA, CSANÁD IMREH, JUDIT NAGY-GYÖRGY, and ZSOLT TUZA. "THE GRAPH-BIN PACKING PROBLEM." International Journal of Foundations of Computer Science 22, no. 08 (December 2011): 1971–93. http://dx.doi.org/10.1142/s012905411100915x.

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We deal with a very general problem: a given graph G is to be "packed" into a host graph H, and we are asked about some natural optimization questions concerning this packing. The problem has never been investigated before in this general form. The input of the problem is a simple graph G = (V, E) with lower and upper bounds on its edges and weights on its vertices. The vertices correspond to items which have to be packed into the vertices (bins) of a host graph, such that each host vertex can accommodate at most L weight in total, and if two items are adjacent in G, then the distance of their host vertices in H must be between the lower and upper bounds of the edge joining the two items. Special cases are bin packing with conflicts, chromatic number, and many more. We give some general structure statements, treat some special cases, and investigate the performance guarantee of polynomial-time algorithms both in the offline and online setting.

34

Brešar, Boštjan, Sandi Klavžar, Douglas F. Rall, and Kirsti Wash. "Packing chromatic number, $$\mathbf (1, 1, 2, 2) $$ ( 1 , 1 , 2 , 2 ) -colorings, and characterizing the Petersen graph." Aequationes mathematicae 91, no. 1 (January 6, 2017): 169–84. http://dx.doi.org/10.1007/s00010-016-0461-8.

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35

Fowler, Katie E., Anjali A. Mandawala, and Darren K. Griffin. "The role of chromosome segregation and nuclear organisation in human subfertility." Biochemical Society Transactions 47, no. 1 (February 7, 2019): 425–32. http://dx.doi.org/10.1042/bst20180231.

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Abstract Spermatogenesis is central to successful sexual reproduction, producing large numbers of haploid motile male gametes. Throughout this process, a series of equational and reductional chromosome segregation precedes radical repackaging of the haploid genome. Faithful chromosome segregation is thus crucial, as is an ordered spatio-temporal ‘dance’ of packing a large amount of chromatin into a very small space. Ergo, when the process goes wrong, this is associated with an improper chromosome number, nuclear position and/or chromatin damage in the sperm head. Generally, screening for overall DNA damage is relatively commonplace in clinics, but aneuploidy assessment is less so and nuclear organisation studies form the basis of academic research. Several studies have focussed on the role of chromosome segregation, nuclear organisation and analysis of sperm morphometry in human subfertility observing significant alterations in some cases, especially of the sex chromosomes. Importantly, sperm DNA damage has been associated with infertility and both extrinsic (e.g. lifestyle) and intrinsic (e.g. reactive oxygen species levels) factors, and while some DNA-strand breaks are repaired, unexpected breaks can cause differential chromatin packaging and further breakage. A ‘healthy’ sperm nucleus (with the right number of chromosomes, nuclear organisation and minimal DNA damage) is thus an essential part of reproduction. The purpose of this review is to summarise state of the art in the fields of sperm aneuploidy assessment, nuclear organisation and DNA damage studies.

36

Chen, Hao. "Ball packings with high chromatic numbers from strongly regular graphs." Discrete Mathematics 340, no. 7 (July 2017): 1645–48. http://dx.doi.org/10.1016/j.disc.2017.03.006.

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37

Pigozzi, M. I., and A. J. Solari. "Equal frequencies of recombination nodules in both sexes of the pigeon suggest a basic difference with eutherian mammals." Genome 42, no. 2 (April 1, 1999): 315–21. http://dx.doi.org/10.1139/g98-137.

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The total number of recombination nodules (RNs) in the autosomal synaptonemal complexes (SCs) is statistically equivalent in oocytes and spermatocytes from the domestic pigeon Columba livia. The distribution on RNs along the three longest autosomes is also equivalent in oocytes and spermatocytes. The numbers of RNs show a linear relationship when plotted against SC length both in oocytes and spermatocytes. On the other hand, the ZW pair shows a single and strictly localized RN near the synaptic termini, but the ZZ pair shows unrestricted location of RNs (average 3.8). The ZW and ZZ pairs of the pigeon are euchromatic and do not show specific chromatin packing at pachytene in either sex. The lack of sex-specific differences in the number and location of RNs in the autosomal bivalents of C. livia and previous data on the chicken, suggest that the regulation of crossing-over is basically different in birds and mammals.Key words: meiosis, genetic recombination, recombination nodules, pigeon gametogenesis.

38

Athey, B. D., M. F. Smith, D. A. Rankert, S. P. Williams, and J. P. Langmore. "The diameters of frozen-hydrated chromatin fibers increase with DNA linker length: evidence in support of variable diameter models for chromatin." Journal of Cell Biology 111, no. 3 (September 1, 1990): 795–806. http://dx.doi.org/10.1083/jcb.111.3.795.

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The diameters of chromatin fibers from Thyone briareus (sea cucumber) sperm (DNA linker length, n = 87 bp) and Necturus maculosus (mudpuppy) erythrocytes (n = 48 bp) were investigated. Soluble fibers were frozen into vitrified aqueous solutions of physiological ionic strength (124 mM), imaged by cryo-EM, and measured interactively using quantitative computer image-processing techniques. Frozen-hydrated Thyone and Necturus fibers had significantly different mean diameters of 43.5 nm (SD = 4.2 nm; SEM = 0.61 nm) and 32.0 nm (SD = 3.0 nm; SEM = 0.36 nm), respectively. Evaluation of previously published EM data shows that the diameters of chromatin from a large number of sources are proportional to linker length. In addition, the inherent variability in fiber diameter suggests a relationship between fiber structure and the heterogeneity of linker length. The cryo-EM data were in quantitative agreement with space-filling double-helical crossed-linker models of Thyone and Necturus chromatin. The data, however, do not support solenoid or twisted-ribbon models for chromatin that specify a constant 30 nm diameter. To reconcile the concept of solenoidal packing with the data, we propose a variable-diameter solid-solenoid model with a fiber diameter that increases with linker length. In principle, each of the variable diameter models for chromatin can be reconciled with local variations in linker length.

39

Widłak, Piotr. "DNA microarrays, a novel approach in studies of chromatin structure." Acta Biochimica Polonica 51, no. 1 (March 31, 2004): 1–8. http://dx.doi.org/10.18388/abp.2004_3592.

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The DNA microarray technology delivers an experimental tool that allows surveying expression of genetic information on a genome-wide scale at the level of single genes--for the new field termed functional genomics. Gene expression profiling--the primary application of DNA microarrays technology--generates monumental amounts of information concerning the functioning of genes, cells and organisms. However, the expression of genetic information is regulated by a number of factors that cannot be directly targeted by standard gene expression profiling. The genetic material of eukaryotic cells is packed into chromatin which provides the compaction and organization of DNA for replication, repair and recombination processes, and is the major epigenetic factor determining the expression of genetic information. Genomic DNA can be methylated and this modification modulates interactions with proteins which change the functional status of genes. Both chromatin structure and transcriptional activity are affected by the processes of replication, recombination and repair. Modified DNA microarray technology could be applied to genome-wide study of epigenetic factors and processes that modulate the expression of genetic information. Attempts to use DNA microarrays in studies of chromatin packing state, chromatin/DNA-binding protein distribution and DNA methylation pattern on a genome-wide scale are briefly reviewed in this paper.

40

Brand, Cara L., and Mia T. Levine. "Functional Diversification of Chromatin on Rapid Evolutionary Timescales." Annual Review of Genetics 55, no. 1 (November 23, 2021): 401–25. http://dx.doi.org/10.1146/annurev-genet-071719-020301.

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Repeat-enriched genomic regions evolve rapidly and yet support strictly conserved functions like faithful chromosome transmission and the preservation of genome integrity. The leading resolution to this paradox is that DNA repeat–packaging proteins evolve adaptively to mitigate deleterious changes in DNA repeat copy number, sequence, and organization. Exciting new research has tested this model of coevolution by engineering evolutionary mismatches between adaptively evolving chromatin proteins of one species and the DNA repeats of a close relative. Here, we review these innovative evolution-guided functional analyses. The studies demonstrate that vital, chromatin-mediated cellular processes, including transposon suppression, faithful chromosome transmission, and chromosome retention depend on species-specific versions of chromatin proteins that package species-specific DNA repeats. In many cases, the ever-evolving repeats are selfish genetic elements, raising the possibility that chromatin is a battleground of intragenomic conflict.

41

Selvam, Kathiresan, John J. Wyrick, and Michael A. Parra. "DNA Repair in Nucleosomes: Insights from Histone Modifications and Mutants." International Journal of Molecular Sciences 25, no. 8 (April 16, 2024): 4393. http://dx.doi.org/10.3390/ijms25084393.

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DNA repair pathways play a critical role in genome stability, but in eukaryotic cells, they must operate to repair DNA lesions in the compact and tangled environment of chromatin. Previous studies have shown that the packaging of DNA into nucleosomes, which form the basic building block of chromatin, has a profound impact on DNA repair. In this review, we discuss the principles and mechanisms governing DNA repair in chromatin. We focus on the role of histone post-translational modifications (PTMs) in repair, as well as the molecular mechanisms by which histone mutants affect cellular sensitivity to DNA damage agents and repair activity in chromatin. Importantly, these mechanisms are thought to significantly impact somatic mutation rates in human cancers and potentially contribute to carcinogenesis and other human diseases. For example, a number of the histone mutants studied primarily in yeast have been identified as candidate oncohistone mutations in different cancers. This review highlights these connections and discusses the potential importance of DNA repair in chromatin to human health.

42

Nguyen, Thinh T., Joanne G. A. Savory, Travis Brooke-Bisschop, Randy Ringuette, Tanya Foley, Bradley L. Hess, Kirk J. Mulatz, Laura Trinkle-Mulcahy, and David Lohnes. "Cdx2 Regulates Gene Expression through Recruitment of Brg1-associated Switch-Sucrose Non-fermentable (SWI-SNF) Chromatin Remodeling Activity." Journal of Biological Chemistry 292, no. 8 (January 12, 2017): 3389–99. http://dx.doi.org/10.1074/jbc.m116.752774.

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The packaging of genomic DNA into nucleosomes creates a barrier to transcription that can be relieved through ATP-dependent chromatin remodeling via complexes such as the switch-sucrose non-fermentable (SWI-SNF) chromatin remodeling complex. The SWI-SNF complex remodels chromatin via conformational or positional changes of nucleosomes, thereby altering the access of transcriptional machinery to target genes. The SWI-SNF complex has limited ability to bind to sequence-specific elements, and, therefore, its recruitment to target loci is believed to require interaction with DNA-associated transcription factors. The Cdx family of homeodomain transcript ion factors (Cdx1, Cdx2, and Cdx4) are essential for a number of developmental programs in the mouse. Cdx1 and Cdx2 also regulate intestinal homeostasis throughout life. Although a number of Cdx target genes have been identified, the basis by which Cdx members impact their transcription is poorly understood. We have found that Cdx members interact with the SWI-SNF complex and make direct contact with Brg1, a catalytic member of SWI-SNF. Both Cdx2 and Brg1 co-occupy a number of Cdx target genes, and both factors are necessary for transcriptional regulation of such targets. Finally, Cdx2 and Brg1 occupancy occurs coincident with chromatin remodeling at some of these loci. Taken together, our findings suggest that Cdx transcription factors regulate target gene expression, in part, through recruitment of Brg1-associated SWI-SNF chromatin remodeling activity.

43

Pebernard, Stephanie, W. Hayes McDonald, Yelena Pavlova, John R. Yates, and Michael N. Boddy. "Nse1, Nse2, and a Novel Subunit of the Smc5-Smc6 Complex, Nse3, Play a Crucial Role in Meiosis." Molecular Biology of the Cell 15, no. 11 (November 2004): 4866–76. http://dx.doi.org/10.1091/mbc.e04-05-0436.

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The structural maintenance of chromosomes (SMC) family of proteins play key roles in the organization, packaging, and repair of chromosomes. Cohesin (Smc1+3) holds replicated sister chromatids together until mitosis, condensin (Smc2+4) acts in chromosome condensation, and Smc5+6 performs currently enigmatic roles in DNA repair and chromatin structure. The SMC heterodimers must associate with non-SMC subunits to perform their functions. Using both biochemical and genetic methods, we have isolated a novel subunit of the Smc5+6 complex, Nse3. Nse3 is an essential nuclear protein that is required for normal mitotic chromosome segregation and cellular resistance to a number of genotoxic agents. Epistasis with Rhp51 (Rad51) suggests that like Smc5+6, Nse3 functions in the homologous recombination based repair of DNA damage. We previously identified two non-SMC subunits of Smc5+6 called Nse1 and Nse2. Analysis of nse1-1, nse2-1, and nse3-1 mutants demonstrates that they are crucial for meiosis. The Nse1 mutant displays meiotic DNA segregation and homologous recombination defects. Spore viability is reduced by nse2-1 and nse3-1, without affecting interhomolog recombination. Finally, genetic interactions shared by the nse mutants suggest that the Smc5+6 complex is important for replication fork stability.

44

Lindstrom, Kimberly C., Jay C. Vary, Mark R. Parthun, Jeffrey Delrow, and Toshio Tsukiyama. "Isw1 Functions in Parallel with the NuA4 and Swr1 Complexes in Stress-Induced Gene Repression." Molecular and Cellular Biology 26, no. 16 (August 15, 2006): 6117–29. http://dx.doi.org/10.1128/mcb.00642-06.

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ABSTRACT The packaging of DNA into chromatin allows eukaryotic cells to organize and compact their genomes but also creates an environment that is generally repressive to nuclear processes that depend upon DNA accessibility. There are several classes of enzymes that modulate the primary structure of chromatin to regulate various DNA-dependent processes. The biochemical activities of the yeast Isw1 ATP-dependent chromatin-remodeling enzyme have been well characterized in vitro, but little is known about how these activities are utilized in vivo. In this work, we sought to discern genetic backgrounds that require Isw1 activity for normal growth. We identified a three-way genetic interaction among Isw1, the NuA4 histone acetyltransferase complex, and the Swr1 histone replacement complex. Transcription microarray analysis revealed parallel functions for these three chromatin-modifying factors in the regulation of TATA-containing genes, including the repression of a large number of stress-induced genes under normal growth conditions. In contrast to a recruitment-based model, we find that the NuA4 and Swr1 complexes act throughout the genome while only a specific subset of the genome shows alterations in transcription.

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Martins, Flavia, Ana L. Machado, Patricia D. Carvalho, Joana Carvalho, Rune Matthiesen, Vadim Backman, and Sergia Velho. "Abstract A006: Chromatin remodeling as a potential epigenetic mechanism of tolerance to KRAS loss." Molecular Cancer Research 21, no. 5_Supplement (May 1, 2023): A006. http://dx.doi.org/10.1158/1557-3125.ras23-a006.

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Abstract KRAS-targeted inhibition yielded promising, yet far from ideal, clinical responses, revealing that cancer cells easily bypass KRAS loss. Therefore, we aim to understand how mutant KRAS cancer cells tolerate so well the loss of a key oncogene to which they were addicted to. KRAS expression was silenced through siRNAs in colorectal cancer (CRC) cell lines that carry KRAS mutations. The proteome characterization was obtained by mass spectrometry and the expression of significantly altered proteins was validated by western blotting. Chromatin states were investigated using electron microscopy. Upon KRAS inhibition, there was a significant reduction in the cell number, accompanied by changes in cell cycle, thus supporting KRAS-dependency. Proteomics analysis revealed that KRAS inhibition-tolerant cells upregulated several proteins associated with the extracellular exosome or nuclear compartments. Molecular function and biological process gene ontology terms revealed an up-regulation of proteins mainly associated with binding activities (RNA, protein, nucleosome, and core promoter binding) as well as gene expression regulation, mRNA splicing and processing, and nucleosome assembly and repositioning. In addition, the proteomics data also revealed an upregulation of proteins associated with active chromatin states. Moreover, KRAS-silenced persister cells also presented alterations in some histone post-translational modifications and in chromatin packing, both suggesting that transcription is impacted. Overall, our results suggest an epigenetic mechanism underlying tolerance to KRAS inhibition that involves chromatin structural changes and transcription alterations, which we are currently pursuing. Citation Format: Flavia Martins, Ana L. Machado, Patricia D. Carvalho, Joana Carvalho, Rune Matthiesen, Vadim Backman, Sergia Velho. Chromatin remodeling as a potential epigenetic mechanism of tolerance to KRAS loss [abstract]. In: Proceedings of the AACR Special Conference: Targeting RAS; 2023 Mar 5-8; Philadelphia, PA. Philadelphia (PA): AACR; Mol Cancer Res 2023;21(5_Suppl):Abstract nr A006.

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Olesen, J. B., and C. A. Heckman. "A 95-nm Spacing in Drosophila Polytene Chromatin." Microscopy and Microanalysis 3, no. 4 (July 1997): 311–20. http://dx.doi.org/10.1017/s1431927697970227.

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Abstract: It has long been debated whether the 30-nm fiber of chromatin is packed in an orderly array. The fiber may be condensed by supercoiling, producing structures of varying diameter. Alternatively, technical problems may have prevented the detection of higher-order structures. We developed a strategy to distinguish between these two possibilities. One potential obstacle to studying the order of packing was the effect of fixatives, dehydrating agents, heat, and embedding polymers on the native structure of chromatin prepared for viewing by electron microscopy. The known tendency of proteins to be degraded by osmium tetroxide and subsequently to be extracted in the conventional protocols for embedding might be particularly damaging. To avoid such denaturants and ensure the retention of proteins in chromatin, the embedding resin HACH was employed. Drosophila mimica polytene chromosomes were thin sectioned, stained with uranyl acetate, and viewed in the transmission electron microscope. Images were digitized and subjected to computerized image processing. Raw data files, containing boundary coordinates of all closed figures in the image, were edited to retain only those regions of interest (ROIs) that exhibited dimensions similar to those of 30-nm fibers in projection views. Euclidean distances between the centroids of such structures were calculated to obtain linear intercepts between recognizable 30-nm fibers. According to stereology theory, the dimensions of a lamellar structure can be determined from the volume distribution function of such intercepts. Therefore, intercept values were pooled for final data files from five processed images of chromatin. The resulting frequency histogram, showing the number of observations at different intercept values, had a sigmoidal inflection that was diagnostic of a major, new spacing at 95 nm. The 95-nm minimum was sandwiched between maxima in the 85 to 90 nm interval and throughout the range 105 to 120 nm. The results suggest that established stereological theory will be a useful tool for investigating the intractable problem of higher-order chromatin structure.

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Jiang, Xuanzhao, Tatiana A. Soboleva, and David J. Tremethick. "Short Histone H2A Variants: Small in Stature but not in Function." Cells 9, no. 4 (April 2, 2020): 867. http://dx.doi.org/10.3390/cells9040867.

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The dynamic packaging of DNA into chromatin regulates all aspects of genome function by altering the accessibility of DNA and by providing docking pads to proteins that copy, repair and express the genome. Different epigenetic-based mechanisms have been described that alter the way DNA is organised into chromatin, but one fundamental mechanism alters the biochemical composition of a nucleosome by substituting one or more of the core histones with their variant forms. Of the core histones, the largest number of histone variants belong to the H2A class. The most divergent class is the designated “short H2A variants” (H2A.B, H2A.L, H2A.P and H2A.Q), so termed because they lack a H2A C-terminal tail. These histone variants appeared late in evolution in eutherian mammals and are lineage-specific, being expressed in the testis (and, in the case of H2A.B, also in the brain). To date, most information about the function of these peculiar histone variants has come from studies on the H2A.B and H2A.L family in mice. In this review, we describe their unique protein characteristics, their impact on chromatin structure, and their known functions plus other possible, even non-chromatin, roles in an attempt to understand why these peculiar histone variants evolved in the first place.

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Barnes, Claire E., David M. English, and Shaun M. Cowley. "Acetylation & Co: an expanding repertoire of histone acylations regulates chromatin and transcription." Essays in Biochemistry 63, no. 1 (April 2019): 97–107. http://dx.doi.org/10.1042/ebc20180061.

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Abstract Packaging the long and fragile genomes of eukaryotic species into nucleosomes is all well and good, but how do cells gain access to the DNA again after it has been bundled away? The solution, in every species from yeast to man, is to post-translationally modify histones, altering their chemical properties to either relax the chromatin, label it for remodelling or make it more compact still. Histones are subject to a myriad of modifications: acetylation, methylation, phosphorylation, ubiquitination etc. This review focuses on histone acylations, a diverse group of modifications which occur on the ε-amino group of Lysine residues and includes the well-characterised Lysine acetylation. Over the last 50 years, histone acetylation has been extensively characterised, with the discovery of histone acetyltransferases (HATs) and histone deacetylases (HDACs), and global mapping experiments, revealing an association of hyperacetylated histones with accessible, transcriptionally active chromatin. More recently, there has been an explosion in the number of unique short chain ‘acylations’ identified by MS, including: propionylation, butyrylation, crotonylation, succinylation, malonylation and 2-hydroxyisobutyrylation. These novel modifications add a range of chemical environments to histones, and similar to acetylation, appear to accumulate at transcriptional start sites and correlate with gene activity.

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Easley, Rebecca, Lawrence Carpio, Irene Guendel, Zachary Klase, Soyun Choi, Kylene Kehn-Hall, John N. Brady, and Fatah Kashanchi. "Human T-Lymphotropic Virus Type 1 Transcription and Chromatin-Remodeling Complexes." Journal of Virology 84, no. 9 (February 17, 2010): 4755–68. http://dx.doi.org/10.1128/jvi.00851-09.

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ABSTRACT Human T-lymphotropic virus type 1 (HTLV-1) encodes the viral protein Tax, which is believed to act as a viral transactivator through its interactions with a variety of transcription factors, including CREB and NF-κB. As is the case for all retroviruses, the provirus is inserted into the host DNA, where nucleosomes are deposited to ensure efficient packaging. Nucleosomes act as roadblocks in transcription, making it difficult for RNA polymerase II (Pol II) to proceed toward the 3′ end of the genome. Because of this, a variety of chromatin remodelers can act to modify nucleosomes, allowing for efficient transcription. While a number of covalent modifications are known to occur on histone tails in HTLV-1 infection (i.e., histone acetyltransferases [HATs], histone deacetylases [HDACs], and histone methyltransferases [HMTs]), evidence points to the use of chromatin remodelers that use energy from ATP hydrolysis to remodel nucleosomes. Here we confirm that BRG1, which is the core subunit of eight chromatin-remodeling complexes, is essential not only for Tax transactivation but also for viral replication. This is especially evident when wild-type infectious clones of HTLV-1 are used. BRG1 associates with Tax at the HTLV-1 long terminal repeat (LTR), and coexpression of BRG1 and Tax results in increased rates of transcription. The interaction of BRG1 with Tax additionally recruits the basal transcriptional machinery and removes some of the core histones from the nucleosome at the start site (Nuc 1). When using the BRG1-deficient cell lines SW13, C33A, and TSUPR1, we observed little viral transcription and no viral replication. Importantly, while these three cell lines do not express detectable levels of BRG1, much of the SWI/SNF complex remains assembled in the cells. Knockdown of BRG1 and associated SWI/SNF subunits suggests that the BRG1-utilizing SWI/SNF complex PBAF is responsible for HTLV-1 nucleosome remodeling. Finally, HTLV-1 infection of cell lines with a knockdown in BRG1 or the PBAF complex results in a significant reduction in viral production. Overall, we concluded that BRG1 is required for Tax transactivation and HTLV-1 viral production and that the PBAF complex appears to be responsible for nucleosome remodeling.

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Lukaszewski, Adam J. "Behavior of Centromeres during Restitution of the First Meiotic Division in a Wheat–Rye Hybrid." Plants 11, no. 3 (January 27, 2022): 337. http://dx.doi.org/10.3390/plants11030337.

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In first division restitution (FDR)-type meiosis, univalents congregate on the metaphase I plate and separate sister chromatids in an orderly fashion, producing dyads with somatic chromosome numbers. The second meiotic division is abandoned. The separation of sister chromatids requires separation of otherwise fused sister centromeres and a bipolar attachment to the karyokinetic spindle. This study analyzed packaging of sister centromeres in pollen mother cells (PMCs) in a wheat–rye F1 hybrid with a mixture of standard reductional meiosis and FDR. No indication of sister centromere separation before MI was observed; such separation was clearly only visible in univalents placed on the metaphase plate itself, and only in PMCs undergoing FDR. Even in the FDR, PMCs univalents off the plate retained fused centromeres. Both the orientation and configuration of univalents suggest that some mechanism other than standard interactions with the karyokinetic spindle may be responsible for placing univalents on the plate, at which point sister centromeres are separated and normal amphitelic interaction with the spindle is established. At this point it is not clear at all what univalent delivery mechanism may be at play in the FDR.