Avoch Slender-billed Curlew
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB36002 | ENA |
REPOSITORIES: ENA
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Project description:Trypanosoma brucei are protozoan parasites that cause sleeping sickness in humans and nagana in cattle. Inside the mammalian host, a quorum sensing-like mechanism coordinates its differentiation from a slender replicative form into a quiescent stumpy form, limiting growth and virulence. SUMOylation is a reversible post-translational modification that enables dynamic regulation of cellular metabolism by the attachment of SUMO monomer or SUMO polymeric chains. We have found that parasites able to conjugate only SUMO monomers are primed for differentiation. This was demonstrated for monomorphic lines that are normally unable to produce stumpy forms in response to quorum sensing signaling in mice, and also for pleomorphic cell lines in which stumpy cells were observed at unusually low parasitemia levels. SUMO chain mutants showed a stumpy compatible transcriptional profile and better competence to differentiate into procyclics. Our study indicates that SUMO depolymerization may represent a coordinated signal triggered during stumpy activation program.
2024-04-03 | GSE261736 | GEO
Project description:In the mammalian bloodstream, proliferative slender forms of T. brucei differentiate into cell cycle-arrested stumpy forms (stumpy-QS) via a quorum sensing mechanism triggered by high parasite density. This transition is thought to protect the host from excessive parasitaemia while preparing the parasites for transmission to the tsetse fly. In this study, we demonstrated that glycerol can also induce the differentiation of slender forms into stumpy forms (stumpy-Glyc), mimicking quorum sensing-induced stumpy forms (stumpy-QS), but with an extended lifespan. Moreover, under tissue-like conditions mimicking the interstitial fluids of adipocytes in the skin (4 mM glucose, 0.25 mM glycerol), glycerol generated proliferative intermediate forms (intermediate-Glyc) capable of differentiating into procyclic forms and establishing infections in tsetse flies. Notably, glycerol also prolonged the survival of quorum-sensing-induced stumpy forms by delaying cell death. Our findings suggest a revised model for T. brucei transmission where quorum sensing controls parasitaemia by producing short-lived stumpy-QS forms, while glycerol secreted by adipocytes in the skin supports the formation of transmissible intermediate-Glyc forms and extends the lifespan of stumpy forms, thus enhancing parasite transmission to tsetse flies.
2026-06-23 | PXD056405 | Pride
Project description:Background: Resistance to trastuzumab remains a common challenge to HER-2 positive breast cancer. Up until now, the underlying mechanism of trastuzumab resistance is still unclear. tRNA-derived small non-coding RNAs (tDRs), a new class of small non-coding RNA (sncRNAs), have been observed to play an important role in cancer progression. However, the relationship between tDRs and trastuzumab resistance is still unknown. Methods: We detected the levels of tDRs expression in normal breast epithelial cell lines, trastuzumab-sensitive and -resistant breast cancer cell lines using high-throughput sequencing. qRT-PCR was conducted to validate the differentially expressed tDRs in serums from trastuzumab-sensitive and -resistant patients. A receiver operating characteristic (ROC) curve analysis was performed to evaluate the power of specific tDRs. Progression-free survival (PFS) was analyzed using Cox-regression. Furthermore, Gene Ontology (GO) and pathway analyses indicated the potential mechanism underlying tDR-mediated trastuzumab resistance. Results: Our sequence results showed that tDRs were differentially expressed in the HBL-100, SKBR3, and JIMT-1 cell lines. tDR-1960 and tDR-1969 were found significantly upregulated in trastuzumab-resistant patients compared to sensitive individuals, and the ROC analysis showed that tDR-1960 and tDR-1969 were correlated with trastuzumab resistance. In a multivariate analysis, higher levels of tDR-1960 and tDR-1969 expression were associated with significantly shorter PFS in patients with metastatic HER-2 positive breast cancer. Additionally, the GO analysis indicated that tDR-1960 and tDR-1969 were mainly involved in the cellular response to drug, which may partially explain the molecular mechanism underlying trastuzumab resistance in HER-2 positive breast cancer. Conclusion: we comprehensively analyzed tDRs in trastuzumab-sensitive and -resistant breast cancer. Our results suggest that tDR-1960 and tDR-1969 play important roles in trastuzumab resistance. Patients with high levels of tDR-1960 and tDR-1969 expression benefitted less from trastuzumab-based therapy than those that express lower-levels of these tDRs. tDR-1960 and tDR-1969 may be potential biomarkers and intervention targets in the clinical treatment of trastuzumab-resistant breast cancer.
2018-06-30 | GSE107473 | GEO
Project description:We have previously shown that the slender form of Trypanosoma (T.) brucei is able to infect teneral tsetse flies, develop to the first fly form, which is the procyclic form, and complete the life cycle in the insect vector (Schuster et al., 2021). Further, analysis of the transmission index (TI; defined as the number of salivary gland infections relative to the number of midgut infections) revealed a higher TI for slender as compared to stumpy forms under laboratory conditions, which included the addition of N-acetyl-glucosamine (NAG) to the infective bloodmeal. These findings challenge the prevailing view of the life cycle, according to which only stumpy forms are considered infective to tsetse flies. Here, we show that slender trypanosomes can infect both male and female tsetse flies, irrespective of their teneral status, in the absence of supplements in the bloodmeal. Additionally, an RNA-sequencing time course was performed on both slender and stumpy cells during their transition into procyclic forms. This analysis revealed that slender and stumpy form trypanosomes remain transcriptionally distinct throughout differentiation into the procyclic form. Furthermore, while the protein associated with differentiation 1 (PAD1) remains essential for the transition, slender cells do not require expression of other hallmark stumpy form traits, such as cell cycle arrest or the shortening of their flagella or microtubule corset. Instead, slender trypanosomes are able to transition directly into procyclic forms. Taken together, these findings demonstrate that while slender cells of T. brucei follow distinct routes to become the procyclic form, they are capable of infecting both teneral and non-teneral tsetse flies, thereby contributing to the transmission and spread of these African parasites.
2026-07-26 | GSE316496 | GEO
Project description:mRNA expression profiles of trypanosomes from two discrete bloodstream form stages of the parasite (slender and stumpy forms), as well as during the transition of the stumpy population to the procyclic life-cycle stage were studied. Our analysis represents the first comparison of in vivo derived pleomorphic slender cells with genetically identical stumpy forms, and a first analysis of the dynamic changes in mRNA profile that accompany the transition to procyclic forms.
2009-07-10 | GSE17026 | GEO
Project description:Comparative analysis of transcriptome profiles of G. arboreum L. cv. and its fuzzy-lintless mutant (ANOI 1960) at 0 and 10 dpa. Cotton is one of the most commercially important fibre crops in the world and used as a source for natural textile fibre and cottonseed oil. The fuzzy-lintless ovules of cotton mutants are ideal source for identifying genes involved in fibre development by comparing with fibre bearing ovules of wild-type. To decipher molecular mechanisms involved in fibre cell development, transcriptome analysis has been carried out by comparing G. arboreum cv. (wild-type) with its fuzzy-lintless mutant (ANOI 1960). Fuzzed-lintless mutant line was generated by back cross breeding between FL and Fl (recurrent parent) lines (personal communication by Dr. I. S. Katageri). Basically Fibre less type was a RIL, first recovered from cross between G.arboreum (linted) and G. anomalum (lint less). This RIL was used as donor parent and crossed with normal arboreum (as recurrent parent) to develop G. arboreum FL and G. arboreum Fl isogenic lines. This G. arboreum Fl line is named as ANOI 1960. Cotton bolls were collected at fibre initiation (0 dpa/days post anthesis) and elongation (10 dpa) and gene expression profiles were analyzed in wild-type and ANOI 1960 mutant using Affymetrix cotton GeneChip Genome array.
2014-11-01 | GSE52432 | GEO