Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA284662 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2037140.fastq.gz | Fastqsanger.gz | |||
| SRR2037150.fastq.gz | Fastqsanger.gz | |||
| SRR2037160.fastq.gz | Fastqsanger.gz | |||
| SRR2037170.fastq.gz | Fastqsanger.gz | |||
| SRR2037180.fastq.gz | Fastqsanger.gz |
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Project description:Using integrated genomics we identify a role for CLEC12A in antibacterial autophagy. Clec12a-/- mice are more susceptible to bacterial infection and CLEC12A deficient cells exhibit impaired antibacterial autophagy. We used transcriptional profilinf to understand the role of CLEC12A in the response to Salmonella and Listeria.
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Project description:Using integrated genomics we identify a role for CLEC12A in antibacterial autophagy. Clec12a-/- mice are more susceptible to bacterial infection and CLEC12A deficient cells exhibit impaired antibacterial autophagy. We used transcriptional profilinf to understand the role of CLEC12A in the response to Salmonella and Listeria. Bone marrow-derived macrophages from WT or Clec12a-/- mice were infected with Salmonella enterica serovar Typhimurium or Listeria monocytogenes. Cells were harvested at 0,3,6, and 24hours post-infection for RNA analysis. Please note that single-end sequencing was performed but two files: R1 files that contained the sample barcodes (19 or 17bp reads) and R2 files that contained the single-end-sequenced 46bp cDNA reads were generated. Since the barcode info is mostly redundant, only R2 reads were submitted (described in 'raw_file_readme.txt').
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Project description:The clear role of autophagy in human inflammatory diseases such as Crohn’s disease was first identified by genome-wide association studies and subsequently dissected in multiple mechanistic studies. ATG16L1 has been particularly well studied in knockout and hypomorph settings as well as models recapitulating the Crohn’s disease-associated T300A polymorphism. Interestingly, ATG16L1 has a single homolog, ATG16L2, which is independently implicated in diseases including Crohn’s disease and systemic lupus erythematosus. However, the contribution of ATG16L2 to canonical autophagy pathways and other cellular functions is poorly understood.To better understand its role, we generate and analyze the first, to our knowledge, ATG16L2 knockout mouse. Our results show that ATG16L1 and ATG16L2 contribute very distinctly to autophagy and cellular ontogeny in myeloid, lymphoid and epithelial lineages. Dysregulation of any of these lineages could contribute to complex diseases like Crohn’s disease and systemic lupus erythematosus, highlighting the value of examining cell-specific effects. We also identify a novel genetic interaction between ATG16L2 and epithelial ATG16L1. These findings are discussed in the context of how these genes may contribute distinctly to human disease.
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Project description:NUP98-NSD1 is one of the most recurring nucleoporin 98 (NUP98) fusions in acute myeloid leukemia (AML). NUP98-NSD1 AML is associated with adverse outcomes and poor response to conventional treatments. However, limited studies have been done to identify new potential targets to develop better treatment approaches. The C-type lectin domain family 12, member A (CLEC12A) is a cell surface receptor that is differentially expressed in leukemic stem cells (LSCs) compared to healthy hematopoietic stem cells (HSCs). We demonstrated a strong overexpression of CLEC12A in both NUP98-NSD1 patients and NUP98-NSD1 transformed murine cells. To understand the role of Clec12a in NUP98-NSD1 AML, we depleted Clec12a expression in NUP98-NSD1+NRASG12D immortalized cells using 3 different sgRNAs targeting 3 different exons. We observed an efficient gene editing in all target sites. NUP98-NSD1+NRASG12D/Clec12a knockout cells showed higher apoptosis and lower colony numbers in vitro compared to NUP98-NSD1+NRASG12D/Clec12a wildtype cells. Importantly, the deletion of Clec12a significantly reduced the leukemic engraftment and prolonged the survival of the NUP98-NSD1+NRASG12D murine model. Our data suggest to further explore CLEC12A as a potential target for the treatment of NUP98-NSD1 AML.
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Project description:Mutations resulting in loss of FAMIN (C13orf31) cause systemic juvenile idiopathic arthritis and very early onset inflammatory bowel disease, while a common I254V substitution increases susceptibility to leprosy and Crohn’s disease. In this study, we compare mRNA transcriptional profiles of bone marrow-derived dendritic cells (DCs) from mice genetically engineered to express Faminp.254I (non-risk), Faminp.254V (risk variant) and Faminp.284R (mutant) at their endogenous loci. We also compare BMDCs from mice lacking FAMIN expression -/- (knockout, KO) with FAMIN+/+ (wild type, WT) mice.
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Project description:Crohn’s disease (CD) is associated with multiple Paneth cell dysfunctions such as altered antimicrobial secretion that relies on autophagy - an essential process controlling the turnover of cellular components. Genome-wide association studies have linked CD to mutations in the ATG16l1 gene, encoding an important component of the autophagy machinery. Patients carrying the ATG16l1 CD risk allele have Paneth cell abnormalities, as reproduced in Atg16l1-deficient mouse models. However, the direct effect of the ATG16L1-deficiency and autophagy-impairment in Paneth cells has not been analysed in detail. To investigate this, we generated a mouse model lacking ATG16L1 specifically in intestinal epithelial cells (Atg16l1△IEC) making these cells impaired in autophagy. Using a 3D small intestinal organoid culture model, which we enriched for Paneth cells and compared the proteomic profiles of organoids derived from the wild-type (WT) and the Atg16l1△IEC mice. We used an integrated computational approach combining protein-protein interaction networks, list of proteins potentially targeted by autophagy and functional information on the proteins with altered protein levels to identify the mechanistic link between autophagy-impairment and disrupted cellular process. 198 (70%) of the 284 altered proteins were more abundant in autophagy-impaired organoids than WT organoids that could be due to a reduced protein turnover. Combining the proteomic dataset with the potential target proteins of selective autophagy proteins revealed that 116 (41%) of the differentially abundant proteins could rely on autophagy-mediated turnover. Taken together, our results suggest that proteins with increased levels in autophagy-impaired background require an autophagy-mediated turnover mechanism, and that their altered levels in CD could affect key cellular processes. Consequently, we pointed out the importance of autophagy in controlling the turnover of proteins relevant in key Paneth cell functions such as exocytosis, apoptosis and DNA damage repair. Our study unravels autophagy-dependent cellular processes of Paneth cells that not directly relies on the autophagy process, rather than a selective protein turnover mechanism. The identified proteins and processes open new avenues for targeted, cell type-specific therapeutic interventions in CD.
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