Further studies on the maternal effect of theo gene in the Mexican axolotl

1972 ◽  
Vol 181 (2) ◽  
pp. 271-280 ◽  
Author(s):  
Robert Briggs
Author(s):  
Larry F. Lemanski ◽  
Eldridge M. Bertke ◽  
J. T. Justus

A recessive mutation has been recently described in the Mexican Axolotl, Ambystoma mexicanum; in which the heart forms structurally, but does not contract (Humphrey, 1968. Anat. Rec. 160:475). In this study, the fine structure of myocardial cells from normal (+/+; +/c) and cardiac lethal mutant (c/c) embryos at Harrison's stage 40 was compared. The hearts were fixed in a 0.1 M phosphate buffered formaldehyde-glutaraldehyde-picric acid-styphnic acid mixture and were post fixed in 0.1 M s-collidine buffered 1% osmium tetroxide. A detailed study of heart development in normal and mutant embryos from stages 25-46 will be described elsewhere.


Author(s):  
Ezzatollah Keyhani ◽  
Larry F. Lemanski ◽  
Sharon L. Lemanski

Energy for sperm motility is provided by both glycolytic and respiratory pathways. Mitochondria are involved in the latter pathway and conserve energy of substrate oxidation by coupling to phosphorylation. During spermatogenesis, the mitochondria undergo extensive transformation which in many species leads to the formation of a nebemkem. The nebemkem subsequently forms into a helix around the axial filament complex in the middle piece of spermatozoa.Immature spermatozoa of axolotls contain numerous small spherical mitochondria which are randomly distributed throughout the cytoplasm (Fig. 1). As maturation progresses, the mitochondria appear to migrate to the middle piece region where they become tightly packed to form a crystalline-like sheath. The cytoplasm in this region is no longer abundant (Fig. 2) and the plasma membrane is now closely apposed to the outside of the mitochondrial layer.


Genetics ◽  
1988 ◽  
Vol 120 (4) ◽  
pp. 977-986
Author(s):  
K J Kemphues ◽  
M Kusch ◽  
N Wolf

Abstract We have analyzed a set of linkage group (LG) II maternal-effect lethal mutations in Caenorhabditis elegans isolated by a new screening procedure. Screens of 12,455 F1 progeny from mutagenized adults resulted in the recovery of 54 maternal-effect lethal mutations identifying 29 genes. Of the 54 mutations, 39 are strict maternal-effect mutations defining 17 genes. These 17 genes fall into two classes distinguished by frequency of mutation to strict maternal-effect lethality. The smaller class, comprised of four genes, mutated to strict maternal-effect lethality at a frequency close to 5 X 10(-4), a rate typical of essential genes in C. elegans. Two of these genes are expressed during oogenesis and required exclusively for embryogenesis (pure maternal genes), one appears to be required specifically for meiosis, and the fourth has a more complex pattern of expression. The other 13 genes were represented by only one or two strict maternal alleles each. Two of these are identical genes previously identified by nonmaternal embryonic lethal mutations. We interpret our results to mean that although many C. elegans genes can mutate to strict maternal-effect lethality, most genes mutate to that phenotype rarely. Pure maternal genes, however, are among a smaller class of genes that mutate to maternal-effect lethality at typical rates. If our interpretation is correct, we are near saturation for pure maternal genes in the region of LG II balanced by mnC1. We conclude that the number of pure maternal genes in C. elegans is small, being probably not much higher than 12.


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