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ARS Home » Plains Area » Houston, Texas » Children's Nutrition Research Center » Research » Publications at this Location » Publication #147780
Title: LOSS OF ORPHAN RECEPTOR GERM CELL NUCLEAR FACTOR (GCNF) FUNCTION RESULTS IN ECTOPIC DEVELOPMENT OF THE TAIL BUD AND A NOVEL POSTERIOR TRUNCATION

Author
item CHUNG, ARTHUR - BAYLOR COLLEGE MED
item KATZ, DEBORAH - BAYLOR COLLEGE MED
item PEREIRA, FRED - BAYLOR COLLEGE MED
item JACKSON, KATHY - BAYLOR COLLEGE MED
item DEMAYO, FRANCESCO - BAYLOR COLLEGE MED
item Cooney, Austin
item O'MALLEY, BERT - BAYLOR COLLEGE MED

Submitted to: Molecular and Cellular Biology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/26/2000
Publication Date: 1/1/2001
Citation: Chung, A.C., Katz, D., Pereira, F.A., Jackson, K.J., Demayo, F.J., Cooney, A., O'Malley, B.W. 2001. Loss of orphan receptor germ cell nuclear factor (gcnf) function results in ectopic development of the tail bud and a novel posterior truncation. Molecular and Cellular Biology. 21(2):663-677.

Interpretive Summary: This is a peer reviewed article that describes the inactivation of a gene GCNF in the mouse. GCNF is a steroid receptor like factor. Loss of this factor leads to loss of mouse fetuses. Analysis of these mouse fetuses showed there was multiple problems.

Technical Abstract: The dynamic embryonic expression of germ cell nuclear factor (GCNF), an orphan nuclear receptor, suggests that it may play an important role during early development. To determine the physiological role of GCNF, we have generated a targeted mutation of the GCNF gene in mice. Germ line mutation of the GCNF gene proves that this orphan nuclear receptor is essential for embryonic survival and normal development. GCNF-/- embryos cannot survive beyond 10.5 days postcoitum (dpc), probably due to cardiovascular failure. Prior to death, GCNF-/- embryos suffer significant defects in posterior development. Unlike GCNF+/+ embryos, GCNF-/- embryos do not turn and remain in a lordotic position, the majority of the neural tube remains open, and the hindgut fails to close. The GCNF-/- embryos also suffer serious defects in trunk development, specifically in somitogenesis, which terminates by 8.75 dpc. The maximum number of somites in GCNF-/- embryos is 13 instead of 25 in the GCNF+/+ embryos. Interestingly, the tailbud of GCNF-/- embryos develops ectopically outside the yolk sac. Indeed, alterations in expression of multiple marker genes were identified in the posterior of GCNF-/- embryos, including the primitive streak, the node and the presomitic mesoderm. These results suggest that GCNF is required for maintenance of somitogenesis and posterior development and is essential for embryonic survival. These results suggest that GCNF regulates a novel and critical developmental pathway involved in normal anteroposterior development.