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M E Flynn

Publications and source records attributed to M E Flynn.

6 recordsLinked to original sources
PubMed1994

Development of cranial flexure and Rathke's pouch in the chick embryo.

Experiments were done to investigate the cause of the cranial (mesencephalic) flexure of the chick brain during stages 10 to 14. Measurements of the length and thickness of the roof and floor of the mesencephalon gave values similar to the values obtained previously by others. The labeling index was determined in the roof and floor of the prosencephalon, mesencephalon, and rhombencephalon as a preliminary measure of cell division. The labeling index was about the same in all regions, and was high enough to suggest that most of the cells were dividing. The labeling indices did not suggest that differential growth was caused by differential rates of cell division in the roof and floor of the mesencephalon. It was found through time lapse photography that the foregut and heart remained stationary along the rostrocaudal axis, whereas the prosencephalon moved rostrally and the mesencephalon underwent flexure. Measurements suggested that the neural tube cranial to the otic primordium grew in volume exponentially at a rate consistent with the labeling index. The rostral tip of the neural tube was observed to be linked to the rostral tip of the foregut by the ectoderm that formed Rathke's pouch at the neural tube and the pharyngeal membrane (prospective stomodeum) at the foregut. As the neural tube grew in length, the link between the neural tube and the foregut did not. We suggest that because of this link, the growing neural tube had to bend around the foregut, forming the cranial flexure, and the ectoderm folded where it attached to the prosencephalon, forming Rathke's pouch.

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PubMed1991

The mechanism of cervical flexure formation in the chick.

Chick embryos, during stages 14 to 25, undergo an arching of the hindbrain and cervical neural tube that is termed cervical flexure. We have found that if the truncus arteriosus is severed during stage 12-13, the embryos survive for more than 24 h and do not show cervical flexure. The embryos have a beating heart, the expected number of somites, and often have discernible wing and leg buds. Light and electron micrographs reveal no histological abnormalities. The percentage of cells that become labeled with tritiated thymidine is close to normal, indicating that most of the cells are healthy. These results suggest that cervical flexure is related to normal morphogenesis of the heart. At stage 10, the heart is almost straight, with the prospective ventricle cranial to the prospective sinus venosus. The heart tube loops between stage 10 and stage 23, first to the right and then caudad, so that the ventricle becomes caudal to the sinus venosus. The heart undergoes these morphogenetic movements autonomously. The truncus arteriosus does not increase in length during caudal movement of the ventricle, so the cervical region is pulled into an arch. Bending of the cervical region into an arch can be prevented in intact embryos by injecting agar into the foregut, so that the foregut cannot bend. However, after about 24 h of further growth, if the axis cannot bend, the truncus begins to leak blood and the embryo dies. We conclude that cervical flexure is a response of the embryonic axis to the morphogenesis of the heart.

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PubMed1988

Mutational analysis of upstream AUG codons of poliovirus RNA.

The 5' untranslated region of poliovirus type 2 Lansing RNA consists of 744 nucleotides containing seven AUG codons which are followed by in-frame termination codons, thus forming short open reading frames (ORFs). To determine the biological significance of these small ORFs, all of the upstream AUG codons were mutated to UUG. The point mutations were introduced into an infectious poliovirus cDNA clone, and RNA transcribed in vitro from the altered cDNA was transfected into HeLa cells to recover the virus. Mutation of AUG 7 resulted in a virus (called R2-5NC-14) with a small-plaque phenotype, whereas mutation of the other six AUG codons produced virus with a wild-type plaque morphology. To determine whether the small-plaque phenotype of R2-5NC-14 was due to altered translational efficiency of the viral mRNA, we constructed chimeric mRNAs containing the 5' noncoding region of poliovirus mRNA fused to the chloramphenicol acetyltransferase (CAT) coding sequence. mRNA containing a mutated AUG 7 codon showed decreased translational efficiency in vitro. The results indicate that the upstream ORFs of poliovirus RNA are not essential for viral replication and do not act as barriers to the translation of poliovirus mRNA. AUG 7 and flanking sequences may play a positive acting role in poliovirus RNA translation.

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