Rax-CreERT2 knock-in mice: a tool for selective and conditional gene deletion in progenitor cells and radial glia of the retina and hypothalamus.
To study gene function in neural progenitors and radial glia of the retina and hypothalamus, we developed a Rax-CreERT2 mouse line in which a tamoxifen-inducible Cre recombinase is inserted into the endogenous Rax locus. By crossing Rax-CreER(T2) with the Cre-dependent Ai9 reporter line, we demonstrate that tamoxifen-induced Cre activity recapitulates the endogenous Rax mRNA expression pattern. During embryonic development, Cre recombinase activity in Rax-CreER(T2) is confined to retinal and hypothalamic progenitor cells, as well as progenitor cells of the posterior pituitary. At postnatal time points, selective Cre recombinase activity is seen in radial glial-like cell types in these organs--specifically Müller glia and tanycytes--as well as pituicytes. We anticipate that this line will prove useful for cell lineage analysis and investigation of gene function in the developing and mature retina, hypothalamus and pituitary.
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
Thomas
T
Pak
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
Sooyeon
S
Yoo
Ana L
AL
Miranda-Angulo
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America; Institute of Medical Research, School of Medicine, Universidad de Antioquia, Medellín, Colombia.
Ana M
AM
Miranda-Angulo
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
Hong
H
Wang
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America; Department of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America; Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America; Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America; Center for High-Throughput Biology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America; Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
Seth
S
Blackshaw
D000818:Animals; D018931:Antineoplastic Agents, Hormonal / Q000494:pharmacology; D015139:Blotting, Southern; D019070:Cell Lineage; D005136:Eye Proteins / Q000502:physiology*; D005260:Female; D017353:Gene Deletion; D018398:Homeodomain Proteins / Q000502:physiology*; D007031:Hypothalamus / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D007124:Immunoenzyme Techniques; D019426:Integrases / Q000378:metabolism*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D009457:Neuroglia / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D011960:Receptors, Estrogen / Q000502:physiology*; D011995:Recombination, Genetic; D012160:Retina / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013234:Stem Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D013629:Tamoxifen / Q000494:pharmacology; D014157:Transcription Factors / Q000502:physiology*
D018931:Antineoplastic Agents, Hormonal; D005136:Eye Proteins; D018398:Homeodomain Proteins; D012333:RNA, Messenger; C105441:Rax protein, mouse; D011960:Receptors, Estrogen; D014157:Transcription Factors; D013629:Tamoxifen; C045073:Cre recombinase; D019426:Integrases