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      Genomic Organization and Control of the Grb7 Gene Family

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          Abstract

          Grb7 and their related family members Grb10 and Grb14 are adaptor proteins, which participate in the functionality of multiple signal transduction pathways under the control of a variety of activated tyrosine kinase receptors and other tyrosine-phosphorylated proteins. They are involved in the modulation of important cellular and organismal functions such as cell migration, cell proliferation, apoptosis, gene expression, protein degradation, protein phosphorylation, angiogenesis, embryonic development and metabolic control. In this short review we shall describe the organization of the genes encoding the Grb7 protein family, their transcriptional products and the regulatory mechanisms implicated in the control of their expression. Finally, the alterations found in these genes and the mechanisms affecting their expression under pathological conditions such as cancer, diabetes and some congenital disorders will be highlighted.

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          Oocyte growth-dependent progression of maternal imprinting in mice.

          Tomohiro Kono, Yayoi Obata, Yuki Shirai … (2006)
          In mammals, some genes categorized as imprinted genes are exclusively expressed either from maternal or paternal allele. This parental-origin-specific gene expression is regulated by epigenetic modification of DNA methylation in differentially methylated region (DMR), which is independently imposed during oogenesis and spermatogenesis. It is known that methylation of DMR in the female germ line is established during oocyte growth phase. However, the cause of the progression of methylation on DMR, due to either aging of mice or growth-size of oocyte was unclear up to now. Here, we analyzed the methylation of DMR for each eight imprinted genes (Igf2r, Lit1, Zac1, Snrpn, Peg1/Mest, Impact, Meg1/Grb10, and H19) by bisulfite sequencing methylation assay, using oocytes from 10 dpp (days post partum), 15 dpp, 20 dpp, and adult mice. To find whether the size of oocytes is the cause of methylation, above oocytes were classified into seven groups (each oocyte diameter ranging from 40 to 75 microm with intervals of 5 microm). The results from juvenile mice oocytes showed that DMR methylation progressed according to oocyte growth each imprinted gene. More than 85% of DMR methylation was achieved for both Igf2r, Zac1 & Lit1 with oocyte size of reaching 55 microm and Snrpn, Peg1/Mest, Impact, and Meg1/Grb10 with oocyte size of reaching 60 microm. Preferential methylation of maternal allele was observed in Zac1 and Peg1/Mest of juvenile oocytes and in Snrpn of juvenile and adult oocytes. The oocyte size-dependent-methylation progressed equally for all three different-age juvenile mice. The size-dependent-methylation was also recognized in the growing oocytes collected from adult mice, although the progress is slightly slower than that of juvenile mice. From these results, we concluded that DNA methylation is established with oocyte size dependent manner, not with aging of mice.
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            Culture of preimplantation mouse embryos affects fetal development and the expression of imprinted genes.

            S Khosla, R Feil, S Khosla … (2001)
            Culture of preimplantation mammalian embryos and cells can influence their subsequent growth and differentiation. Previously, we reported that culture of mouse embryonic stem cells is associated with deregulation of genomic imprinting and affects the potential for these cells to develop into normal fetuses. The purpose of our current study was to determine whether culture of preimplantation mouse embryos in a chemically defined medium (M16) with or without fetal calf serum (FCS) can affect their subsequent development and imprinted gene expression. Only one third of the blastocysts that had been cultured from two-cell embryos in M16 medium complemented with FCS developed into viable Day 14 fetuses after transfer into recipients. These M16 + FCS fetuses were reduced in weight as compared with controls and M16 fetuses and had decreased expression of the imprinted H19 and insulin-like growth factor 2 genes associated with a gain of DNA methylation at an imprinting control region upstream of H19. They also displayed increased expression of the imprinted gene Grb10. The growth factor receptor binding gene Grb7, in contrast, was strongly reduced in its expression in most of the M16 + FCS fetuses. No alterations were detected for the imprinted gene MEST: Preimplantation culture in the presence of serum can influence the regulation of multiple growth-related imprinted genes, thus leading to aberrant fetal growth and development.
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              Disruption of the imprinted Grb10 gene leads to disproportionate overgrowth by an Igf2-independent mechanism.

              Marika Charalambous, Florentia Smith, William R Bennett … (2003)
              To investigate the function of the Grb10 adapter protein, we have generated mice in which the Grb10 gene was disrupted by a gene-trap insertion. Our experiments confirm that Grb10 is subject to genomic imprinting with the majority of Grb10 expression arising from the maternally inherited allele. Consistent with this, disruption of the maternal allele results in overgrowth of both the embryo and placenta such that mutant mice are at birth approximately 30% larger than normal. This observation establishes that Grb10 is a potent growth inhibitor. In humans, GRB10 is located at chromosome 7p11.2-p12 and has been associated with Silver-Russell syndrome, in which approximately 10% of those affected inherit both copies of chromosome 7 from their mother. Our results indicate that changes in GRB10 dosage could, in at least some cases, account for the severe growth retardation that is characteristic of Silver-Russell syndrome. Because Grb10 is a signaling protein capable of interacting with tyrosine kinase receptors, we tested genetically whether Grb10 might act downstream of insulin-like growth factor 2, a paternally expressed growth-promoting gene. The result indicates that Grb10 action is essentially independent of insulin-like growth factor 2, providing evidence that imprinting acts on at least two major fetal growth axes in a manner consistent with parent-offspring conflict theory.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Curr Genomics
                Journal ID (publisher-id): CG
                Title: Current Genomics
                Publisher: Bentham Science Publishers Ltd.
                ISSN (Print): 1389-2029
                ISSN (Electronic): 1875-5488
                Publication date (Print): March 2008
                Volume: 9
                Issue: 1
                Pages: 60-68
                Affiliations
                []Instituto de Investigaciones Biomédicas, Consejo Superior de Investigaciones Científicas & Universidad Autónoma de Madrid. Arturo Duperier 4, E-28029 Madrid, Spain
                Author notes
                [* ]Address correspondence to this author at the Instituto de Investigaciones Biomédicas, Consejo Superior de Investigaciones Científicas and Universidad Autónoma de Madrid. Arturo Duperier 4, E-28029 Madrid, Spain; Tel: 34-91-585-4424; Fax: 34-91-585-4401; E-mail: antonio.villalobo@ 123456iib.uam.es
                Article
                Publisher ID: CG-9-60
                DOI: 10.2174/138920208783884847
                PMC ID: 2674303
                PubMed ID: 19424485
                SO-VID: 1807ba07-d059-48f1-bcc8-e8754384095a
                Copyright © ©2008 Bentham Science Publishers Ltd.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.5/) which permits unrestrictive use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 9 January 2008
                Date revision received : 20 February 2008
                Date accepted : 21 February 2008
                Categories
                Subject: Article

                ScienceOpen disciplines: Genetics
                Keywords: grb7,grb10,adaptor proteins,uniparental disomy,congenital disorders,splice variants.,diabetes,genetic imprinting,grb14,cancer
                Data availability:
                ScienceOpen disciplines: Genetics
                Keywords: grb7, grb10, adaptor proteins, uniparental disomy, congenital disorders, splice variants., diabetes, genetic imprinting, grb14, cancer

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