Identification of erythroid‐enriched gene expression in the mouse embryonic yolk sac using microdissected cells

Redmond, Latasha C.; Dumur, Catherine I.; Archer, Kellie J.; Haar, Jack L.; Lloyd, Joyce A.

doi:10.1002/dvdy.21426

Cited by 20 publications

(32 citation statements)

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“…Characterization of ErGFPcre (EpoRCre in ) knock-in and Myc fl/fl mutant mice (provided by U. Klingmüller, S. Philipsen, and F. Alt) was previously described (17,33 Ϫ/Ϫ , KLF2 Ϫ/Ϫ , and KLF1 Ϫ/Ϫ KLF2 Ϫ/Ϫ embryonic yolk sacs, which were embedded in freezing medium and cryosectioned for laser capture microdissection (LCM) (63).…”

Section: Animalsmentioning

confidence: 99%

“…Ϫ/Ϫ , and 3 KLF1 Ϫ/Ϫ KLF2 Ϫ/Ϫ samples were used for Affymetrix 430A 2.0 microarray assays (63)(64)(65).…”

Section: Expression Profiling Of Klf1mentioning

confidence: 99%

“…These genes were chosen for further analysis because their P values were relatively low (Table 2), and except for that of the gene for Ddx3x, their expression is enriched in E9.5 yolk sac embryonic erythroid cells compared to epithelial cells, based on our previous data (63). The selected genes encode GMP reductase (Gmpr); Pklr; Tfrc; DEAD/H box polypeptide 3, X linked (Ddx3x); Myc; cathepsin E (Ctse); and cold shock protein A (Csda).…”

Section: Expression Profiling Of Klf1mentioning

confidence: 99%

“…Microarray gene expression assays showed that in KLF2 Ϫ/Ϫ mouse E9.5 erythroid precursor cells, 89 genes are significantly downregulated, including genes enriched in erythroid cells (63), such as those that encode the cell signaling factors CD24a antigen, cytotoxic T-lymphocyte-associated protein 2 alpha (Ctla2␣), adenylate cyclase 7, and reelin (60). KLF2 can partially compensate for KLF1 function in regulating the mouse embryonic ␤-globin genes, because KLF1 and KLF2 double knockout (KO) mice die earlier in development at a critical phase of primitive erythropoiesis (5).…”

mentioning

confidence: 99%

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Krüppel-Like Factor 1 (KLF1), KLF2, and Myc Control a Regulatory Network Essential for Embryonic Erythropoiesis

Pang

Lemsaddek

Alhashem

et al. 2012

Molecular and Cellular Biology

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Section: Animalsmentioning

confidence: 99%

“…Ϫ/Ϫ , and 3 KLF1 Ϫ/Ϫ KLF2 Ϫ/Ϫ samples were used for Affymetrix 430A 2.0 microarray assays (63)(64)(65).…”

Section: Expression Profiling Of Klf1mentioning

confidence: 99%

Section: Expression Profiling Of Klf1mentioning

confidence: 99%

mentioning

confidence: 99%

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Krüppel-Like Factor 1 (KLF1), KLF2, and Myc Control a Regulatory Network Essential for Embryonic Erythropoiesis

Pang

Lemsaddek

Alhashem

et al. 2012

Molecular and Cellular Biology

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“…Many KLFs are expressed during erythropoiesis. These include Klf1, Klf2, Klf3, Klf6, and Klf10 (Redmond et al, 2008). Klf1, the founding member of the KLF family (Miller & Bieker, 1993), is erythroid-specific and is essential for definitive erythropoiesis (Nuez et al, 1995, Perkins et al, 1995.…”

Section: Introductionmentioning

confidence: 99%

Investigating the Molecular Pathogenesis of Inherited Childhood Anaemia

Ilsley¹

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Krüppel-like factors (KLFs) are a group of 17 transcription factors with diverse functions such as early embryo patterning, organogenesis and tissue homoeostasis. All 17 members contain highlyconserved DNA-binding domains consisting of three C-terminal C2H2-type zinc fingers. This high level of conservation allows all members of the KLF family to bind to a 9 base pair CACCC-box DNA sequence (CCM CRC CCN) which is commonly found in many tissue-specific gene promoters and enhancers. The activity of each member of the KLF family is largely determined by a more variable N-terminal domain through which they interact with co-factors such as p300 and C-terminal binding protein 2 (CtBP2).Many KLFs are often expressed in the same cells. In these situations, they can form transcriptional networks where they coordinate to control developmental programs. For example, KLF2, KLF4, and KLF5 work redundantly in embryonic stem cells where they regulate key pluripotency genes such as Nanog to maintain the 'stemness' of the cell. Multiple KLFs are expressed during erythropoiesis, the ongoing production of red blood cells, where it is likely that they form transcriptional networks to control differentiation.Krüppel-like factor 1 (KLF1) is an erythroid-specific transcription factor that is responsible for coordinating the expression of a large cohort of genes required for nearly all aspects of erythropoiesis. As the founding member of the KLF group, KLF1 contains three C-terminal C2H2-type zinc fingers that bind to DNA and an N-terminal proline-rich activation domain that interacts with co-factors to initiate transcription of target genes.This thesis investigates the molecular mechanisms of Klf1 binding specificity to DNA and how this is affected by mutations, and by competition between family members.A disease that is known as Congenital Dyserythropoietic anaemia type IV (CDAIV) is a rare autosomal-dominant inherited erythrocyte disorder characterised by ineffective erythropoiesis and haemolysis. CDAIV is caused by a point mutation in the second zinc finger of KLF1 which results in substitution of an amino acid predicted to bind to DNA.A mouse carrying a point mutation in the corresponding amino acid residue in murine Klf1 to that mutated in CDAIV patients has been previously generated in an ENU screen. This mouse displays a semi-dominant haemolytic anaemia and is named 'Nan' for 'neonatal anaemia'. The Nan mouse shares a similar phenotype to that of patients with CDAIV and hereditary spherocytosis.Incredibly, both the 'Nan' and CDAIV mutations cause disease which is far more severe than that of commonly occurring Klf1 haploinsufficiency.ii ChIP-seq analysis in cell lines developed to model Klf1 mutations identified aberrant DNAbinding events genome-wide for both the mouse 'Nan' mutation and the human CDAIV mutation.Next-generation sequencing of newly-synthesised RNA (4sU-RNA-seq) reveals ectopic transcriptional consequences of this aberrant binding. Novel sequence specificity of the mutant protein was confirmed by performi...

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Nonneuronal roles for the reelin signaling pathway

Khialeeva

Carpenter

2016

Developmental Dynamics

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The reelin signaling pathway has been established as an important regulator of cell migration during development of the central nervous system, and disruptions in reelin signaling alter the positioning of many types of neurons. Reelin is a large extracellular matrix glycoprotein and governs cell migration through activation of multiple intracellular signaling events by means of the receptors ApoE receptor 2 (ApoER2) and very low density lipoprotein receptor (VLDLR), and the intracellular adaptor protein Disabled-1 (Dab1). Earlier studies reported expression of reelin in nonneuronal tissues, but the functions of this signaling pathway outside of the nervous system have not been studied until recently. A large body of evidence now suggests that reelin functions during development and disease of multiple nonneuronal tissues. This review addresses recent advances in the field of nonneuronal reelin signaling. Developmental Dynamics 246:217-226,

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Identification of erythroid‐enriched gene expression in the mouse embryonic yolk sac using microdissected cells

Cited by 20 publications

References 49 publications

Krüppel-Like Factor 1 (KLF1), KLF2, and Myc Control a Regulatory Network Essential for Embryonic Erythropoiesis

Krüppel-Like Factor 1 (KLF1), KLF2, and Myc Control a Regulatory Network Essential for Embryonic Erythropoiesis

Investigating the Molecular Pathogenesis of Inherited Childhood Anaemia

Nonneuronal roles for the reelin signaling pathway

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