An E2F Binding-Deficient Rb1 Protein Partially Rescues Developmental Defects Associated with Rb1 Nullizygosity

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Published inMolecular and Cellular Biology Vol. 26; no. 4; pp. 1527 - 1537
Main Authors Sun, Huifang, Chang, Yanjie, Schweers, Brett, Dyer, Michael A., Zhang, Xiaojing, Hayward, Simon W., Goodrich, David W.
Format Journal Article
LanguageEnglish
Published United States American Society for Microbiology 01.02.2006
Taylor & Francis
Subjects
Alleles
Amino Acid Substitution
Animals
Base Sequence
Cell Cycle
Congenital Abnormalities - genetics
Congenital Abnormalities - pathology
DNA - genetics
E2F Transcription Factors - metabolism
Female
Fetal Development - genetics
Fetal Development - physiology
Homozygote
Male
Mice
Mice, Knockout
Mice, Mutant Strains
Mutagenesis, Site-Directed
Pregnancy
Recombinant Proteins - genetics
Recombinant Proteins - metabolism
Retina - abnormalities
Retinoblastoma Protein - deficiency
Retinoblastoma Protein - genetics
Retinoblastoma Protein - metabolism
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Abstract Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue MCB About MCB Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy MCB RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0270-7306 Online ISSN: 1098-5549 Copyright © 2014 by the American Society for Microbiology.   For an alternate route to MCB .asm.org, visit: MCB       
AbstractList Rb1 is essential for normal embryonic development, as null mice die in midgestation with widespread unscheduled cell proliferation. Rb1 protein (pRb) mediates cell cycle control by binding E2F transcription factors and repressing expression from E2F-dependent promoters. An increasing amount of evidence suggests that pRb loss also compromises cellular differentiation. Since differentiation is often dependent on cell cycle exit, it is currently unclear whether the effects of pRb on differentiation are an indirect consequence of pRb/E2F-mediated cell cycle control or whether they reflect direct cell-type-specific pRb functions. We have mutated Rb1 in the mouse to express a protein (R654W) specifically deficient in binding E2F1, E2F2, and E2F3. R654W mutant embryos exhibit cell cycle defects the same as those of Rb1 null embryos, reinforcing the importance of the interactions of pRb with E2F1, E2F2, and E2F3 for cell cycle control. However, R654W embryos survive at least 2 days longer than Rb1 null embryos, and increased life span is associated with improved erythrocyte and fetal liver macrophage differentiation. In contrast, R654W pRb does not rescue differentiation defects associated with pRb-deficient retinae. These data indicate that Rb1 makes important cell-type-specific contributions to cellular differentiation that are genetically separable from its general ability to stably bind E2F1, E2F2, and E2F3 and regulate the cell cycle.
Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue MCB About MCB Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy MCB RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0270-7306 Online ISSN: 1098-5549 Copyright © 2014 by the American Society for Microbiology.   For an alternate route to MCB .asm.org, visit: MCB       
Rb1 is essential for normal embryonic development, as null mice die in midgestation with widespread unscheduled cell proliferation. Rb1 protein (pRb) mediates cell cycle control by binding E2F transcription factors and repressing expression from E2F-dependent promoters. An increasing amount of evidence suggests that pRb loss also compromises cellular differentiation. Since differentiation is often dependent on cell cycle exit, it is currently unclear whether the effects of pRb on differentiation are an indirect consequence of pRb/E2F-mediated cell cycle control or whether they reflect direct cell-type-specific pRb functions. We have mutated Rb1 in the mouse to express a protein (R654W) specifically deficient in binding E2F1, E2F2, and E2F3. R654W mutant embryos exhibit cell cycle defects the same as those of Rb1 null embryos, reinforcing the importance of the interactions of pRb with E2F1, E2F2, and E2F3 for cell cycle control. However, R654W embryos survive at least 2 days longer than Rb1 null embryos, and increased life span is associated with improved erythrocyte and fetal liver macrophage differentiation. In contrast, R654W pRb does not rescue differentiation defects associated with pRb-deficient retinae. These data indicate that Rb1 makes important cell-type-specific contributions to cellular differentiation that are genetically separable from its general ability to stably bind E2F1, E2F2, and E2F3 and regulate the cell cycle.
Author Xiaojing Zhang
David W. Goodrich
Huifang Sun
Michael A. Dyer
Brett Schweers
Yanjie Chang
Simon W. Hayward
AuthorAffiliation Department of Pharmacology & Therapeutics, Roswell Park Cancer Institute, Buffalo, New York 14263, 1 Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, 2 Departments of Urologic Surgery and Cancer Biology, Vanderbilt University Medical Center, Nashville, Tennessee 37235 3
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Corresponding author. Mailing address: Department of Pharmacology & Therapeutics, Roswell Park Cancer Institute, Elm & Carlton Streets, Buffalo, NY 14263. Phone: (716) 845-4506. Fax: (716) 845-8857. E-mail: david.goodrich@roswellpark.org.
These authors contributed equally to the work.
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Snippet Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley...
Rb1 is essential for normal embryonic development, as null mice die in midgestation with widespread unscheduled cell proliferation. Rb1 protein (pRb) mediates...
Rb1 is essential for normal embryonic development, as null mice die in midgestation with widespread unscheduled cell proliferation. Rb1 protein (pRb) mediates...
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SubjectTerms Alleles
Amino Acid Substitution
Animals
Base Sequence
Cell Cycle
Congenital Abnormalities - genetics
Congenital Abnormalities - pathology
DNA - genetics
E2F Transcription Factors - metabolism
Female
Fetal Development - genetics
Fetal Development - physiology
Homozygote
Male
Mice
Mice, Knockout
Mice, Mutant Strains
Mutagenesis, Site-Directed
Pregnancy
Recombinant Proteins - genetics
Recombinant Proteins - metabolism
Retina - abnormalities
Retinoblastoma Protein - deficiency
Retinoblastoma Protein - genetics
Retinoblastoma Protein - metabolism
Title An E2F Binding-Deficient Rb1 Protein Partially Rescues Developmental Defects Associated with Rb1 Nullizygosity
URI http://mcb.asm.org/content/26/4/1527.abstract
https://www.tandfonline.com/doi/abs/10.1128/MCB.26.4.1527-1537.2006
https://www.ncbi.nlm.nih.gov/pubmed/16449662
https://search.proquest.com/docview/17487348
https://pubmed.ncbi.nlm.nih.gov/PMC1367194
Volume 26
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