Defects of embryonic organogenesis resulting from targeted disruption of the N-myc gene in the mouse | doi.page

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Defects of embryonic organogenesis resulting from targeted disruption of the N-myc gene in the mouse

Development1993Vol. 117(4), pp. 1445–1455

Citations Over TimeTop 10% of 1993 papers

Shoji Sawai, Akihiko Shimono, Yoshio Wakamatsu, Cynthia Palmes, Kazunori Hanaoka, Hisato Kondoh

Abstract

The highest expression of the N-myc gene occurs during embryonic organogenesis in the mouse ontogeny, with the peak of expression around embryonic day 9.5. Homozygous N-myc-deficient mice, produced by germline transmission of a disrupted allele in ES cells, developed normally to day 10.5, indicating dispensability of N-myc expression in the earlier period, but later accumulated organogenic abnormalities and died around day 11.5. The most notable abnormalities were found in the limb bud, visceral organs (lung, stomach, liver and heart) and the central/peripheral nervous systems, and were highly correlated with the site of N-myc expression. The limb buds and the lungs excised from N-myc-deficient mutant embryos were placed in culture to allow their development to stages beyond the point of death of the embryos. Analyses indicated that the mutant limbs failed to develop distal structures and the development of bronchi from the trachea was defective in the lungs. The latter defect was largely corrected by addition of fetal calf serum to the culture medium, suggesting that an activity missing in the mutant lung was replenished by a component of the serum. The phenotype of N-myc-deficient mutant embryos indicated requirement of the N-myc function in many instances of tissue interactions in organogenesis and also in cell-autonomous regulation of tissue maturation.

Citations Over TimeTop 10% of 1993 papers

Abstract

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