Disease relevance of stm

• The treatment of mice with indomethacin lowered Trypanosoma brucei parasitemia 1 to 2 log10 because it quickly promoted the differentiation of rapidly dividing long, slender trypanosomes into short, stumpy forms that do not divide in the mammal but do develop a functional mitochondrion and the ability to infect the tsetse [1].
• The shapes of scapulae and basi-occipital bones from three genetically distinct achondroplastic mutants and one osteopetrotic mutant in the mouse (achondroplasia, brachymorphic, stumpy and grey lethal), and appropriate controls, have been compared using Fourier analysis and multivariate statistical techniques [2].

High impact information on stm

• A novel selection regime for differentiation defects demonstrates an essential role for the stumpy form in the life cycle of the African trypanosome [3].
• However, the attenuated growth of the Delta-glycophosphatidyl inositol-phospholipase C DiD-1 cells in mice permitted the expression of stumpy characteristics in this previously monomorphic cell line, and concomitantly their ability to differentiate efficiently was restored [3].
• These results show that the level of some mitochondrial transcripts is developmentally regulated in bloodstream trypanosomes and suggest that the stumpy bloodstream trypanosomes accumulate mitochondrial transcripts prior to development of a functional mitochondrion [4].
• Transcripts from three other mitochondrial genes, cytochrome b and subunits I and II of cytochrome oxidase, are undetectable in the slender trypanosomes and increase in the stumpy trypanosomes to levels approaching those in trypanosomes from 26 degrees C cultures [4].
• This suggests a function of ZFK associated with the trypanosomes' decision between either cell cycle progression, as slender bloodstream form, or differentiation to the non-dividing stumpy form [5].

Chemical compound and disease context of stm

• These ascofuranone-induced short stumpy forms were morphologically analogous to the stumpy forms 2 days after peak parasitemia of pleomorphic clone of T. b. brucei GUTat 3 [6].

Biological context of stm

• Cell kinetics of growth cartilage in stumpy: a new chondrodystrophic mutant in the mouse [7].
• It was found that the major factor responsible for the reduced growth rate in stumpy up to 21 days was the small hypertrophic cell height, while cell proliferation zone size and labelling indices were of minor importance [7].
• These results suggest that the change in proportions of slender and stumpy forms at the peak of a parasitaemic wave results from slender forms being more susceptible to complement-mediated killing as the antibody response develops [8].
• Cell density triggers slender to stumpy differentiation of Trypanosoma brucei bloodstream forms in culture [9].
• Down regulation of S-adenosyl-L-methionine decarboxylase activity of Trypanosoma brucei during transition from long slender to short stumpy-like forms in axenic culture [10].

Anatomical context of stm

• Abnormal cartilage from the mandibular condyle of stumpy (stm) mutant mice [11].
• The proximal growth plates of the tibiae in normal and stumpy mice aged 10-41 days were studied [7].
• In an opsonization assay, no differences were observed between slender and stumpy forms in the extent to which they attached to macrophages in an antibody-dependent manner [8].
• Surface antigen biosynthesis and fate in monomorphic and pleomorphic Trypanosoma brucei was examined to assess how slender and stumpy form T. brucei parasites present their variant specific glycoprotein (VSG) to the host immune system [12].
• Little difference was observed between IMP density of long slender and short stumpy form body membranes: IMP's were more abundant on the protoplasmic face (PF) than on the exoplasmic face (EF) [13].

Associations of stm with chemical compounds

• Stumpy populations emanating from these infections transformed rapidly and synchronously into dividing procyclic forms when triggered with cis-aconitate and a temperature shift [14].
• Short stumpy trypanosomes hydrolyse z-Phe-Arg-AMC 12 fold more actively than either long slenders or procyclics [15].
• We propose a new model for the Stumpy Induction Factor-induced slender to stumpy transformation of Trypanosoma brucei gambiense cells in immunosuppressed mice [16].
• A subclone which did give rise to stumpy forms in mice, was less virulent and did stimulate an antibody response specific for the trypanosome surface glycoprotein [17].
• If mice were infected with a highly virulent trypanosome clone (ETat 1.10), which does not normally transform from long slender (LS) to short stumpy (SS) forms, DFMO treatment caused SS transformation to occur on days 3-4 [18].

Regulatory relationships of stm

• During experimental T. brucei infection in BALB/c mice, the anti-HSP60 response was induced when parasites differentiated into stumpy forms [19].

Other interactions of stm

• In these cultures, AdoMetDC activity decreased with a t1/2 of 7 h during transition from long slender to short stumpy-like forms as soon as the stationary phase was reached [10].

Analytical, diagnostic and therapeutic context of stm

• We have used immunoblotting, immunofluorescence, and cryoimmunoelectron microscopy to study CB1-glycoprotein expression as long, slender bloodstream forms of pleomorphic T. b. brucei and T. b. gambiense transform through intermediate stages into short, stumpy forms [20].

References