Presence of an unusually high concentration of an ubiquitinated histone-like protein inTrypanosoma cruzi

Reverol, Lorena; Chirinos, Mayel; Henriquez, Diana

doi:10.1002/(sici)1097-4644(19970915)66:4<433::aid-jcb2>3.0.co;2-m

Cited by 3 publications

(4 citation statements)

References 36 publications

(38 reference statements)

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“…This will be in line with other authors who postulate a strong contribution of post‐translational modifications of histone tails, such as acetylation phosphorylation, and ubiquitination in the modulation of chromatin structure and function [Li et al, 1993; Cheung et al, 2000]. In T. cruzi , Reverol et al [1997] have demonstrated the presence of an unusually high concentration of ubiquitinated histone‐like proteins.…”

Section: Discusionsupporting

confidence: 87%

“…Histone proteins of T.cruzi have been extensively characterized by Toro and co‐workers [Toro and Galanti, 1988, 1990; Toro et al, 1992, 1993] and Reverol et al [1997]. These authors characterized T.cruzi histones by their banding pattern in different gel systems, their solubility properties, and amino acid composition.…”

Section: Discusionmentioning

confidence: 99%

“…Subsequently, in the hindgut, epimastigotes differentiate into metacyclic trypomastigotes, which can infect mammalian host cells when the excrements of the infected bugs come in contact with the skin of humans [De Souza, 1984]. The complex changes observed during the life cycle of T. cruzi could be the results of adaptative modifications in gene expression [González‐Pino et al, 1999], which might be accompanied by modifications of chromatin structure [Reverol et al, 1997].…”

mentioning

confidence: 99%

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Differences in the nuclear chromatin among various stages of the life cycle of Trypanosoma cruzi

Spadiliero

Sánchez

Slezynger

et al. 2002

J of Cellular Biochemistry

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Trypanosoma cruzi is the etiological agent of Chagas. Although the nuclear chromatin of this parasite is organized in the form of nucleosome filaments, its chromatin is physically and enzymatically fragile, and no condensation into chromosomes occurs during mitosis. All previous investigations have been carried out with epimastigote form in its proliferate stage. It is not known whether these differences in chromatin structure are also found in the non-proliferate stationary epimastigote forms and in tissue derived trypomastigotes. Our results confirm that chromatin of logarithmic epimastigotes presents limited compaction when increasing salt concentrations from 1 to 100 mM NaCl, and no 30-nm fibers were formed. Contrary to these results, non-proliferative forms of the parasites showed a pattern of compactation similar to that observed in rat liver chromatin, where solenoids of 30-nm fibers are formed at 100-mM NaCl. In accordance with these results, digestion of the nuclear chromatin with DNase I revealed that the chromatin of logarithmic phase epimastigotes was more accessible to the enzyme. We conclude from these results that structural differences in the chromatin exist not only between T. cruzi and higher eukaryotes but also among various forms of the parasite. The functional significance of these differences are currently under investigation.

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Section: Discusionsupporting

confidence: 87%

Section: Discusionmentioning

confidence: 99%

mentioning

confidence: 99%

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Differences in the nuclear chromatin among various stages of the life cycle of Trypanosoma cruzi

Spadiliero

Sánchez

Slezynger

et al. 2002

J of Cellular Biochemistry

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“…Future directions that may hold particular relevance in this case should include a closer look at histone ubiquitination in trypanosomes. An unusually high concentration of a ubiquitinated histone‐like protein has been observed in T. cruzi (Reverol et al ., 1997). This may be significant as the ubiquitination of yeast H2B has been linked to telomere‐associated gene silencing (Sun and Allis, 2002).…”

Section: Histone Marks and Modifying Enzymesmentioning

confidence: 95%

Histones and histone modifications in protozoan parasites

2006

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SummaryProtozoan parasites are early branching eukaryotes causing significant morbidity and mortality in humans and livestock. Single-celled parasites have evolved complex life cycles, which may involve multiple host organisms, and strategies to evade host immune responses. Consequently, two key aspects of virulence that underlie pathogenesis are parasite differentiation and antigenic variation, both of which require changes in the expressed genome. Complicating these requisite alterations in the parasite transcriptome is chromatin, which serves as a formidable barrier to DNA processes including transcription, repair, replication and recombination. Considerable progress has been made in the study of chromatin dynamics in other eukaryotes, and there is much to be gained in extending these analyses to protozoan parasites. Much of the work completed to date has focused on histone acetylation and methylation in the apicomplexans and trypanosomatids. As we describe in this review, such studies provide a unique vantage point of the evolutionary picture of eukaryotic cell development, and reveal unique phenomena that could be exploited pharmacologically to treat protozoal diseases.

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