B-myb Is Required for Inner Cell Mass Formation at an Early Stage of Development

Tanaka, Yasunori; Patestos, Nikos P.; Maekawa, Tomoko; Ishii, Shunsuke

doi:10.1074/jbc.274.40.28067

Cited by 149 publications

(130 citation statements)

References 42 publications

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“…These WISH results confirmed this microarray-based finding. It is reported that Mybl2 −/− mice die at around E4.5 -E6.5 and in vitro culture of Mybl2 −/− blastocyst indicates that Mybl2 is required for ICM formation (Tanaka et al, 1999). The ICM-predominant expression of Mybl2 is thus consistent with this null phenotype.…”

Section: All Stage Analysis Of Selected Genesmentioning

confidence: 59%

High-throughput screen for genes predominantly expressed in the ICM of mouse blastocysts by whole mount in situ hybridization

Yoshikawa

Piao

Zhong

et al. 2006

Gene Expression Patterns

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Mammalian preimplantation embryos provide an excellent opportunity to study temporal and spatial gene expression in whole mount in situ hybridization (WISH). However, large-scale studies are made difficult by the size of the embryos (∼60 μm diameter) and their fragility. We have developed a chamber system that allows parallel processing of embryos without the aid of a microscope. We first selected 91 candidate genes that were transcription factors highly expressed in blastocysts, and more highly expressed in embryonic (ES) than in trophoblast (TS) stem cells. We then used the WISH to identify 48 genes expressed predominantly in the ICM and to follow several of these genes in all seven preimplantation stages. The ICM-predominant expressions of these genes suggest their involvement in the pluripotency of embryonic cells. This system provides a useful tool to a systematic genome-scale analysis of preimplantation embryos.

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Section: All Stage Analysis Of Selected Genesmentioning

confidence: 59%

High-throughput screen for genes predominantly expressed in the ICM of mouse blastocysts by whole mount in situ hybridization

Yoshikawa

Piao

Zhong

et al. 2006

Gene Expression Patterns

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“…B-Myb-null mutant mice die at E4.5-6.5 due to failure of the inner cell mass to grow (Tanaka et al, 1999). Although the precise cause of this lethality is not known, evidence is emerging that B-Myb depletion in mouse ES cells (the in vitro counterpart of the inner cell mass) results in mitotic failure (Tarasov et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

A Lin-9 complex is recruited by B-Myb to activate transcription of G2/M genes in undifferentiated embryonal carcinoma cells

2009

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It has recently been discovered that cell-cycle gene transcription is regulated by a core complex named LINC that switches from a transcriptionally repressive complex in G 0 -G 1 with the p130 or p107 pocket proteins and E2F4 to a transcriptionally active complex in S-G 2 containing B-Myb. We have studied the function of LINC in F9 embryonal carcinoma cells, which are distinguished by a rapid cell cycle resulting from an extremely short G 1 phase. We show that suppressing expression of the LINC component, Lin-9, in F9 cells causes arrest in mitosis, and we have used this system to screen for transcriptional targets. In these cells, B-Myb was found in complexes with Lin-9 and several other LINC constituents, however, the pocket proteins did not associate with LINC unless F9 cells were differentiated. Lin-9 and B-Myb were both required for transcription of G 2 /M genes such as Cyclin B1 and Survivin. Moreover, B-Myb was demonstrated to recruit Lin-9 to the Survivin promoter through multiple Myb-binding sites. The demonstration that a B-Myb/ LINC complex is vital for progression through mitosis in cells lacking a G 1 /S checkpoint has implications for both undifferentiated embryonal cells and for cancers in which pocket protein function is compromised.

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“…This data imply that a large fraction of the human population is carrier of B-MYB alleles that might be associated with a reduced risk of developing neoplastic disease. Oncogene (2008Oncogene ( ) 27, 2929Oncogene ( -2933doi:10.1038/sj.onc.1210947;published online 19 November 2007 Keywords: transcription; neuroblastoma; colon cancer; leukaemia; apoptosis B-MYB is a putative proto-oncogene required for mammalian development and involved in cell proliferation and survival (Oh and Reddy, 1999;Tanaka et al, 1999;Sala, 2005). Although there is still no evidence of its direct involvement in human cancer, several studies have revealed that B-MYB is either amplified or overexpressed in different human malignancies, while its expression in neuroblastoma patients correlates with poor survival (Raschella et al, 1999;Forozan et al, 2000;Tanner et al, 2000;Bar-Shira et al, 2002).…”

mentioning

confidence: 99%

Isolation and functional assessment of common, polymorphic variants of the B-MYB proto-oncogene associated with a reduced cancer risk

Schwab¹,

Bussolari

Corvetta

et al. 2007

Oncogene

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The B-MYB proto-oncogene is a transcription factor belonging to the MYB family that is frequently overexpressed or amplified in different types of human malignancies. While it is suspected that B-MYB plays a role in human cancer, there is still no direct evidence of its causative role. Looking for mutations of the B-MYB gene in human cell lines and primary cancer samples, we frequently isolated two nonsynonymous B-MYB polymorphic variants (rs2070235 and rs11556379). Compared to the wild-type protein, the B-MYB isoforms display altered conformation, impaired regulation of target genes and decreased antiapoptotic activity, suggesting that they are hypomorphic variants of the major allele. Importantly, the B-MYB polymorphisms are common; rs2070235 and rs11556379 are found, depending on the ethnic background, in 10-50% of human subjects. We postulated that, if B-MYB activity is important for transformation, the presence of common, hypomorphic variants might modify cancer risk. Indeed, the B-MYB polymorphisms are underrepresented in 419 cancer patients compared to 230 controls (odds ratio 0.53; (95%) confidence interval 0.385-0.755; P ¼ 0.001). This data imply that a large fraction of the human population is carrier of B-MYB alleles that might be associated with a reduced risk of developing neoplastic disease.

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B-myb Is Required for Inner Cell Mass Formation at an Early Stage of Development

Cited by 149 publications

References 42 publications

High-throughput screen for genes predominantly expressed in the ICM of mouse blastocysts by whole mount in situ hybridization

High-throughput screen for genes predominantly expressed in the ICM of mouse blastocysts by whole mount in situ hybridization

A Lin-9 complex is recruited by B-Myb to activate transcription of G2/M genes in undifferentiated embryonal carcinoma cells

Isolation and functional assessment of common, polymorphic variants of the B-MYB proto-oncogene associated with a reduced cancer risk

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