scholarly journals Post-transcriptional control of nuclear-encoded cytochrome oxidase subunits in Trypanosoma brucei: evidence for genome-wide conservation of life-cycle stage-specific regulatory elements

2006 ◽  
Vol 34 (18) ◽  
pp. 5312-5324 ◽  
Author(s):  
Matthew Mayho ◽  
Katelyn Fenn ◽  
Paul Craddy ◽  
Susan Crosthwaite ◽  
Keith Matthews
Keyword(s):  
Life Cycle ◽  
Cytochrome Oxidase ◽  
Trypanosoma Brucei ◽  
Transcriptional Control ◽  
Regulatory Elements ◽  
Life Cycle Stage ◽  
Genome Wide

Developmental aspects of uridine addition within mitochondrial transcripts of Trypanosoma brucei

1988 ◽  
Vol 8 (3) ◽  
pp. 1259-1265
Author(s):  
J E Feagin ◽  
K Stuart
Keyword(s):  
Life Cycle ◽  
Cytochrome Oxidase ◽  
Trypanosoma Brucei ◽  
Cytochrome B ◽  
Respiratory System ◽  
Life Cycle Stage ◽  
Stage Specificity ◽  
Life Cycle Stages ◽  
Mitochondrial Transcripts ◽  
Cytochrome Oxidase Ii

The mitochondrial respiratory system is absent in slender bloodstream forms of Trypanosoma brucei, incomplete in stumpy bloodstream forms, and complete in procyclic (insect) forms. The steady-state abundance of transcripts of some mitochondrially encoded components of the respiratory system correlates with its differential expression in different life cycle stages. Recently, it was reported that uridines which are not encoded in the genome are added to cytochrome b and cytochrome oxidase II transcripts. We now report that the (U)+ transcripts of both genes are found in procyclic forms and to some degree in stumpy forms but are absent in slender forms. The uridine additions to cytochrome oxidase II correct a frameshift in the gene and presumably allow production of a full-length protein, whereas those added to cytochrome b create an in-frame AUG which extends the N terminus of the predicted protein by 20 amino acids. The stage specificity of uridine additions to these transcripts thus reflects the life cycle stage during which the protein products would be used. Transcripts of MURF2, a gene of unknown function, have additional uridines in both slender and procyclic forms which create two in-frame AUGs. MURF2 transcripts additionally differ from the DNA sequence in ways which cannot be explained by uridine addition alone, implying that other processes alter these transcripts.

scholarly journals Developmental aspects of uridine addition within mitochondrial transcripts of Trypanosoma brucei.

1988 ◽  
Vol 8 (3) ◽  
pp. 1259-1265 ◽  
Author(s):  
J E Feagin ◽  
K Stuart
Keyword(s):  
Life Cycle ◽  
Cytochrome Oxidase ◽  
Trypanosoma Brucei ◽  
Cytochrome B ◽  
Respiratory System ◽  
Life Cycle Stage ◽  
Stage Specificity ◽  
Life Cycle Stages ◽  
Mitochondrial Transcripts ◽  
Cytochrome Oxidase Ii

The mitochondrial respiratory system is absent in slender bloodstream forms of Trypanosoma brucei, incomplete in stumpy bloodstream forms, and complete in procyclic (insect) forms. The steady-state abundance of transcripts of some mitochondrially encoded components of the respiratory system correlates with its differential expression in different life cycle stages. Recently, it was reported that uridines which are not encoded in the genome are added to cytochrome b and cytochrome oxidase II transcripts. We now report that the (U)+ transcripts of both genes are found in procyclic forms and to some degree in stumpy forms but are absent in slender forms. The uridine additions to cytochrome oxidase II correct a frameshift in the gene and presumably allow production of a full-length protein, whereas those added to cytochrome b create an in-frame AUG which extends the N terminus of the predicted protein by 20 amino acids. The stage specificity of uridine additions to these transcripts thus reflects the life cycle stage during which the protein products would be used. Transcripts of MURF2, a gene of unknown function, have additional uridines in both slender and procyclic forms which create two in-frame AUGs. MURF2 transcripts additionally differ from the DNA sequence in ways which cannot be explained by uridine addition alone, implying that other processes alter these transcripts.

scholarly journals Genome-wide binding and mechanistic analyses of Smchd1-mediated epigenetic regulation

2015 ◽  
Vol 112 (27) ◽  
pp. E3535-E3544 ◽  
Author(s):  
Kelan Chen ◽  
Jiang Hu ◽  
Darcy L. Moore ◽  
Ruijie Liu ◽  
Sarah A. Kessans ◽  
...  
Keyword(s):  
Epigenetic Regulation ◽  
Transcriptional Control ◽  
Regulatory Elements ◽  
Ctcf Binding ◽  
Dna And Rna ◽  
Chromatin Interactions ◽  
Genome Wide ◽  
Binding Factor ◽  
Structural Maintenance Of Chromosomes ◽  
Hinge Domain

Structural maintenance of chromosomes flexible hinge domain containing 1 (Smchd1) is an epigenetic repressor with described roles in X inactivation and genomic imprinting, but Smchd1 is also critically involved in the pathogenesis of facioscapulohumeral dystrophy. The underlying molecular mechanism by which Smchd1 functions in these instances remains unknown. Our genome-wide transcriptional and epigenetic analyses show that Smchd1 binds cis-regulatory elements, many of which coincide with CCCTC-binding factor (Ctcf) binding sites, for example, the clustered protocadherin (Pcdh) genes, where we show Smchd1 and Ctcf act in opposing ways. We provide biochemical and biophysical evidence that Smchd1–chromatin interactions are established through the homodimeric hinge domain of Smchd1 and, intriguingly, that the hinge domain also has the capacity to bind DNA and RNA. Our results suggest Smchd1 imparts epigenetic regulation via physical association with chromatin, which may antagonize Ctcf-facilitated chromatin interactions, resulting in coordinated transcriptional control.

Coordination of the Cell Cycle in Trypanosomes

2019 ◽  
Vol 73 (1) ◽  
pp. 133-154 ◽  
Author(s):  
Richard J. Wheeler ◽  
Keith Gull ◽  
Jack D. Sunter
Keyword(s):  
Cell Cycle ◽  
Life Cycle ◽  
Trypanosoma Brucei ◽  
Cross Talk ◽  
Life Cycle Stage ◽  
Life Cycles ◽  
Complex Life Cycles ◽  
Cell Divisions ◽  
Proliferative Cell

Trypanosomes have complex life cycles within which there are both proliferative and differentiation cell divisions. The coordination of the cell cycle to achieve these different divisions is critical for the parasite to infect both host and vector. From studying the regulation of the proliferative cell cycle of the Trypanosoma brucei procyclic life cycle stage, three subcycles emerge that control the duplication and segregation of ( a) the nucleus, ( b) the kinetoplast, and ( c) a set of cytoskeletal structures. We discuss how the clear dependency relationships within these subcycles, and the potential for cross talk between them, are likely required for overall cell cycle coordination. Finally, we look at the implications this interdependence has for proliferative and differentiation divisions through the T. brucei life cycle and in related parasitic trypanosomatid species.

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