title: Abnormal erythroid differentiation in neonatal bcl-6-deficient mice.
abstract: OBJECTIVE
  The bcl-6 proto-oncogene is ubiquitously expressed in various tissues. Since we found out the smaller number of TER119(+) cells in the spleen of neonatal bcl-6-deficient (bcl-6(-/-)) mice compared with that of control (bcl-6(+/+)) littermates, we studied functions of bcl-6 in differentiation of erythroid lineage cells.
  
  
  METHODS
  Erythroblasts in the definitive erythropoiesis were separated into four subsets using anti-TER119 and anti-CD71 mAbs. The cell number and property of these four subsets in spleens of neonatal bcl-6(+/+) and bcl-6(-/-) mice were examined using a flow cytometry.
  
  
  RESULTS
  bcl-6 mRNA expression was detected in the TER119(high)CD71(high) subset, which is morphologically equivalent to basophilic erythroblasts, by reverse-transcribed polymerase chain reaction. High percentages of cells in the TER119(low)CD71(high) and TER119(high)CD71(high) subsets were in the cell cycle. The cell number of the TER119(high)CD71(high) subset in the spleen and the percentage of reticulocytes in the peripheral blood of neonatal bcl-6(-/-) mice were significantly lower than those of neonatal bcl-6(+/+) mice. However, the percentage of apoptotic cells and that of cells in the cell cycle in the TER119(high)CD71(high) subset of bcl-6(-/-) mice were similar to those of bcl-6(+/+) mice.
  
  
  CONCLUSIONS
  bcl-6 detected in the TER119(high)CD71(high) subset of erythroblasts in the spleen of neonatal mice may be required to retain the erythroblasts in the cell proliferation stage.
authors.affiliation: Department of Developmental Genetics (H2), Graduate School of Medicine, Chiba University, Chiba, Japan.
authors.forename: Sadaki
authors.initials: S
authors.lastname: Asari
authors.forename: Akemi
authors.initials: A
authors.lastname: Sakamoto
authors.forename: Seiji
authors.initials: S
authors.lastname: Okada
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Ohkubo
authors.forename: Masafumi
authors.initials: M
authors.lastname: Arima
authors.forename: Masahiko
authors.initials: M
authors.lastname: Hatano
authors.forename: Yoshikazu
authors.initials: Y
authors.lastname: Kuroda
authors.forename: Takeshi
authors.initials: T
authors.lastname: Tokuhisa
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D015703:Antigens, CD / Q000032:analysis; D000944:Antigens, Differentiation, B-Lymphocyte / Q000032:analysis; D001789:Blood Group Antigens / Q000032:analysis; D002454:Cell Differentiation; D049109:Cell Proliferation; D004268:DNA-Binding Proteins / Q000172:deficiency / Q000502:physiology*; D004900:Erythroblasts / Q000166:cytology; D004906:Erythrocyte Count; D004912:Erythrocytes / Q000166:cytology* / Q000502:physiology; D004920:Erythropoiesis; D051379:Mice; D018345:Mice, Knockout; D011518:Proto-Oncogene Proteins / Q000172:deficiency / Q000502:physiology*; D051560:Proto-Oncogene Proteins c-bcl-6; D011990:Receptors, Transferrin; D012156:Reticulocytes / Q000166:cytology; D013154:Spleen / Q000166:cytology; D014157:Transcription Factors / Q000172:deficiency / Q000502:physiology*
chemical_list: D015703:Antigens, CD; D000944:Antigens, Differentiation, B-Lymphocyte; D001789:Blood Group Antigens; C068126:CD71 antigen; D004268:DNA-Binding Proteins; D011518:Proto-Oncogene Proteins; D051560:Proto-Oncogene Proteins c-bcl-6; D011990:Receptors, Transferrin; C489122:TER-119 antigen, mouse; D014157:Transcription Factors