TY - JOUR
T1 - Expression and activity of L-Myc in normal mouse development
AU - Hatton, Kimi S.
AU - Mahon, Kathleen
AU - Chin, Lynda
AU - Chiu, Fung Chow
AU - Lee, Han Woong
AU - Peng, Damin
AU - Morgenbesser, Sharon D.
AU - Horner, James
AU - DePinho, Ronald A.
PY - 1996/4
Y1 - 1996/4
N2 - To determine the role of L-Myc in normal mammalian development and its functional relationship to other members of the Myc family, we determined the normal patterns of L-myc gene expression in the developing mouse by RNA in situ hybridization and assessed the phenotypic impact of L-Myc deficiency produced through standard gene targeting methodology. L-myc transcripts were detected in the developing kidney and lung as well as in both the proliferative and the differentiative zones of the brain and neural tube. Despite significant expression of L-myc in developing mouse tissues, homozygous null L-myc mice were found to be viable, reproductively competent, and represented in expected frequencies from heterozygous matings. A detailed histological survey of embryonic and adult tissues, characterization of an embryonic neuronal marker, and measurement of cellular proliferation in situ did not reveal any congenital abnormalities. The lack of an apparent phenotype associated with L-Myc deficiency indicates that L-Myc is dispensable fur gross morphological development and argues against a unique role for L-Myc in early central nervous system development as had been previously suggested. Although overlapping expression patterns among myc family members raise the possibility of complementation of L-Myc deficiency by other Myc oncoproteins, compensatory changes in the levels of c- and/or N- myc transcripts were not detected in homozygous null L-myc mice.
AB - To determine the role of L-Myc in normal mammalian development and its functional relationship to other members of the Myc family, we determined the normal patterns of L-myc gene expression in the developing mouse by RNA in situ hybridization and assessed the phenotypic impact of L-Myc deficiency produced through standard gene targeting methodology. L-myc transcripts were detected in the developing kidney and lung as well as in both the proliferative and the differentiative zones of the brain and neural tube. Despite significant expression of L-myc in developing mouse tissues, homozygous null L-myc mice were found to be viable, reproductively competent, and represented in expected frequencies from heterozygous matings. A detailed histological survey of embryonic and adult tissues, characterization of an embryonic neuronal marker, and measurement of cellular proliferation in situ did not reveal any congenital abnormalities. The lack of an apparent phenotype associated with L-Myc deficiency indicates that L-Myc is dispensable fur gross morphological development and argues against a unique role for L-Myc in early central nervous system development as had been previously suggested. Although overlapping expression patterns among myc family members raise the possibility of complementation of L-Myc deficiency by other Myc oncoproteins, compensatory changes in the levels of c- and/or N- myc transcripts were not detected in homozygous null L-myc mice.
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U2 - 10.1128/MCB.16.4.1794
DO - 10.1128/MCB.16.4.1794
M3 - Article
C2 - 8657155
AN - SCOPUS:0029981848
SN - 0270-7306
VL - 16
SP - 1794
EP - 1804
JO - Molecular and cellular biology
JF - Molecular and cellular biology
IS - 4
ER -