scholarly journals The Relationship between DNA Replication and Human Genome Organization

2009 ◽  
Vol 26 (4) ◽  
pp. 729-741 ◽  
Author(s):  
A. Necsulea ◽  
C. Guillet ◽  
J.-C. Cadoret ◽  
M.-N. Prioleau ◽  
L. Duret
Keyword(s):  
Dna Replication ◽  
Human Genome ◽  
Genome Organization ◽  
The Relationship

Drosophila melanogaster H1 histone is phosphorylated stably

1987 ◽  
Vol 7 (11) ◽  
pp. 4118-4121
Author(s):  
D A Talmage ◽  
M Blumenfeld
Keyword(s):  
Drosophila Melanogaster ◽  
Salivary Gland ◽  
Dna Replication ◽  
Cultured Cells ◽  
Phosphorylation Site ◽  
Developmentally Regulated ◽  
Central Domain ◽  
Salivary Gland Cells ◽  
Adult Head ◽  
The Relationship

Phosphorylation of histone H1 is developmentally regulated in Drosophila spp. It cannot be detected in preblastoderm embryos or polytene salivary gland cells, but in cellular blastoderm, postblastoderm embryo, and amitotic adult head nuclei, it occurs with a frequency of roughly 4 x 10(5) molecules per nucleus. We used pulse-labeling to study the relationship between H1 synthesis and modification in cultured cells. These results reveal that the H1-associated phosphate is stable and suggest that Drosophila H1 is synthesized, translocated to the nucleus, associated with chromatin, and then phosphorylated. Partial tryptic digestion of Drosophila H1 revealed that the phosphorylation site is located within the globular, central domain of the protein. Thus, the developmentally regulated phosphorylation of Drosophila H1 presents two contrasts with previously studied H1 phosphorylation. It is not correlated with DNA replication, and it is located in the central domain of the protein.

Genetics and genetic instability in cancer

2019 ◽  
pp. 43-55
Author(s):  
Mark A. Glaire ◽  
David N. Church
Keyword(s):  
Dna Replication ◽  
Human Genome ◽  
Genomic Instability ◽  
Genetic Instability ◽  
Important Determinant ◽  
Human Cancer ◽  
Deleterious Mutations ◽  
Cellular Processes ◽  
Repair Mechanisms ◽  
Genomic Damage

"The Integrity"of the human genome is under continual threat from endogenous and exogenous mutagens, and as a result of errors introduced during DNA replication. As the lesions generated by these processes, if left uncorrected, may lead to deleterious mutations, cells employ several sophisticated mechanisms to both prevent and repair such genomic damage. Failure of these repair mechanisms, leading to genomic instability, is common in cancer, and has even been suggested to be a universal characteristic of malignancy. This chapter outlines these cellular processes and reviews the both the mechanisms and consequences of their dysregulation in human cancer. It also highlights the emerging evidence suggesting that genomic instability is an important determinant of tumour behaviour. Finally, it discusses the possibility that targeting genomic instability may benefit patients with genomically unstable tumours in the clinic.

scholarly journals Topologically associated domains enriched for lineage-specific genes reveal expression-dependent nuclear topologies during myogenesis

2016 ◽  
Vol 113 (12) ◽  
pp. E1691-E1700 ◽  
Author(s):  
Daniel S. Neems ◽  
Arturo G. Garza-Gongora ◽  
Erica D. Smith ◽  
Steven T. Kosak
Keyword(s):  
Gene Regulation ◽  
Genome Organization ◽  
Spatial Organization ◽  
Potential Role ◽  
Spatial Distance ◽  
Linear Distribution ◽  
Myotube Formation ◽  
Topologically Associated Domains ◽  
The Relationship ◽  
Lineage Specific Genes

The linear distribution of genes across chromosomes and the spatial localization of genes within the nucleus are related to their transcriptional regulation. The mechanistic consequences of linear gene order, and how it may relate to the functional output of genome organization, remain to be fully resolved, however. Here we tested the relationship between linear and 3D organization of gene regulation during myogenesis. Our analysis has identified a subset of topologically associated domains (TADs) that are significantly enriched for muscle-specific genes. These lineage-enriched TADs demonstrate an expression-dependent pattern of nuclear organization that influences the positioning of adjacent nonenriched TADs. Therefore, lineage-enriched TADs inform cell-specific genome organization during myogenesis. The reduction of allelic spatial distance of one of these domains, which contains Myogenin, correlates with reduced transcriptional variability, identifying a potential role for lineage-specific nuclear topology. Using a fusion-based strategy to decouple mitosis and myotube formation, we demonstrate that the cell-specific topology of syncytial nuclei is dependent on cell division. We propose that the effects of linear and spatial organization of gene loci on gene regulation are linked through TAD architecture, and that mitosis is critical for establishing nuclear topologies during cellular differentiation.

Human genome organization

1995 ◽  
Vol 5 (3) ◽  
pp. 315-322 ◽  
Author(s):  
Katheleen Gardiner
Keyword(s):  
Human Genome ◽  
Genome Organization

scholarly journals Mammalian Septins Nomenclature

2002 ◽  
Vol 13 (12) ◽  
pp. 4111-4113 ◽  
Author(s):  
Ian G. Macara ◽  
Richard Baldarelli ◽  
Christine M. Field ◽  
Michael Glotzer ◽  
Yasuhide Hayashi ◽  
...  
Keyword(s):  
Human Genome ◽  
Gene Product ◽  
Genome Organization ◽  
Splice Variants ◽  
Gene Products ◽  
Gene Nomenclature ◽  
Nomenclature System ◽  
Nomenclature Committee ◽  
Human And Mouse ◽  
Mouse Genomic

There are 10 known mammalian septin genes, some of which produce multiple splice variants. The current nomenclature for the genes and gene products is very confusing, with several different names having been given to the same gene product and distinct names given to splice variants of the same gene. Moreover, some names are based on those of yeast or Drosophilaseptins that are not the closest homologues. Therefore, we suggest that the mammalian septin field adopt a common nomenclature system, based on that adopted by the Mouse Genomic Nomenclature Committee and accepted by the Human Genome Organization Gene Nomenclature Committee. The human and mouse septin genes will be namedSEPT1–SEPT10 and Sept1–Sept10, respectively. Splice variants will be designated by an underscore followed by a lowercase “v” and a number, e.g., SEPT4_v1.

Sign in / Sign up

Export Citation Format

Share Document