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Expression of the Jimpy Gene in the Spinal Cords of Heterozygous Female Mice

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Expression of the Jimpy Gene in the Spinal Cords of Heterozygous Female Mice The Journal of Neuroscience October 1986, 6(10): 2802-2812 Expression of the Jimpy Gene in the Spinal Cords of Heterozygous Female Mice. I. An Early Myelin Deficit Followed by Compensation William P. Bartlett and Robert P. Skoff Department of Anatomy, Wayne State University School of Medicine, Detroit, Michigan 48201 The jimpy mutation results in severe hypomyelination through- carrier is a mosaic and should express the jimpy gene according out the CNS of hemizygous male mice. In the female carrier of to Lyon’s hypothesis of X-chromosome inactivation (Lyon, 196 1, the jimpy gene, partial hypomyelination is predicted as a con- 1972). Expression of the jimpy gene in the female carrier was sequence of genetic mosaicism resulting from random X-chro- first described in the optic nerve by Skoff and Nowicki-Mont- mosome inactivation. The spinal cord of the female carrier was gomery (198 1). In the optic nerve of the young carrier, patches studied morphologically to determine (1) if hypomyelination is of unmyelinated axons are adjacent to areas of myelinated fibers. present, (2) the manner in which a possible myelin deficit is These patches of unmyelinated fibers may encompass a large expressed, and (3) the extent, if any, of compensation. portion of the cross-sectional area of the optic nerve and persist The spinal cords of 14- to 15-d-old heterozygotes were found into adulthood (R. P. Skoff, unpublished observations). to be hypomyelinated. A deficit of 31% in the amount of myelin In contrast to the nerve, patches of unmyelinated axons are as compared to controls was detected in these young carriers by not obvious in the brain and spinal cord (Rosenfeld and Fried- point-counting stereology. By the end of the first month the rich, 1984; Skoff, 1982). In biochemical studies, however, mea- deficit was 12%, and after the fifth month complete recovery surements of myelin components are reduced 30-60% in the had occurred. These results demonstrate that the neuroglial cells young female carrier (Benjamins et al., 1984; Kerner and Car- are capable of compensating totally for the jimpy defect over a son, 1984). Morphologically, a reduced amount of myelin has several month period. been demonstrated in the anterior commissure of the young The reduction in the amount of myelin at 2 weeks postnatally carrier (Rosenfeld and Friedrich, 1984). However, it is unknown is due to the ensheathment of fewer axons than normal and the from these studies how the hypomyelination is expressed in the formation of myelin sheaths that are thinner than normal. It is spinal cord and brain. Is the hypomyelination due to the en- not due to a significant reduction in amount of axoplasm and a sheathment of fewer axons than normal, or to myelin sheaths corresponding decrease in amount of myelin. This finding in- that are thinner than normal? Another explanation for the deficit dicates that overall brain development is not retarded but that may be an overall retardation in brain development leading to expression of the jimpy gene selectively affects the glial cells. a reduction in the amount of axoplasm in the carrier and a Our morphologic studies also suggest that the neuron is not the corresponding reduction in myelin. target of the jimpy mutation. One line of evidence for this state- The available evidence suggests that the deficit in the brain ment is that virtually all the axons are partially ensheathed, a and spinal cord of the carrier is temporary and that the neuroglia condition that should not occur if 50% of the neurons are de- are capable of compensating for the hypomyelination (Bartlett fective in the mosaic. and Skoff, 1984; Benjamins et al., 1984; Rosenfeld and Fried- The coexistence of both normal and defective cells within the rich, 1984; Skoffet al., 1985). The mechanisms utilized in com- same cell population and the apparent sparing of the neuron pensation have not been explored. makes the female carrier of the jimpy gene an excellent model We have undertaken the following study to answer 3 ques- for studying mechanisms of compensation and plasticity of neu- tions: (1) Is the spinal cord of the heterozygote hypomyelinated? roglial cells. (2) If so, in what manner is the deficit expressed? (3) Is the mosaic capable of compensation? The results from this study Jimpy (jp) is a sex-linked recessive gene that produces severe show that there is considerably less myelin in the spinal cords hypomyelination throughout the CNS of hemizygous male mice of 14-d-old carriers than controls. We provide evidence clearly (Sidman et al., 1964). The affected jimpy males begin to exhibit showing that in the spinal cord the carrier is capable of recover- body tremors by postnatal day 10 and usually die before day ing completely from the early deficiency in myelination. 30. The cause of the myelin deficit is not known although there have been numerous biochemical (e.g., Barbarese et al., 1979; Materials and Methods Campagnoni et al., 1972; Carnow et al., 1984; Hogan, 1977; Becauseof thejimpy gene’s lethal nature, it is maintained in the female Meier et al., 1974) and morphological (e.g., Farkas-Bargeton et in the heterozygous state with Tabby (Ta), a closely linked mutation al., 1972; Meier and Bischoff, 1975; Privat et al., 1982; Skoff, modifying coat color (crossover frequency between Ta and jp is about 1976, 1982; Wolf et al., 1981) studies. 15%; Wolf and Holden, 1969). Breeding pairs consisting of Tabby males Due to the lethal nature of the jimpy gene in the males, the (Ta+/Y) and female carriers of Tabby and jimpy (Tajp/++) were ob- tained from Jackson Laboratories (Bar Harbor, ME). Because of cross- mutation is maintained in the heterozygous female. The female overs in the female parent, 4 different genotypes were obtained among the female offspring, parental Tajp/Ta+ and Ta+/++; crossovers are Received June 3, 1985; revised Mar. 10, 1986; accepted Apr. 1, 1986. Ta+/Ta+ and +jp/Ta+. This work was supported by NIH Research Grants NS 15338, NS 18883, and Mosaics were tentatively identified by the Tabby light brown fur coat NS 18898. and kink at the end of their tails (Tajp/Ta+) or the alternating bands of Correspondence should be addressed to William P. Bartlett, Ph.D., Department light and dark fur strips down their back (+jp/Ta+). Definitive diagnosis of Anatomy, Wayne State University School of Medicine, 540 East Canfield for expression of the jimpy gene was made by the presence of patches Avenue, Detroit, MI 4820 1. of hypomyelinated axons in l-pm-thick plastic sections of the optic Copyright 0 1986 Society for Neuroscience 0270-6474/86/102802-l 1$02.00/O nerve. Carriers ofthe jimpy gene can be identified at all ages, and patches 2802 The Journal of Neuroscience Myelin Deficit in Jimpy Females 2803 of hypomyelination have been observed in 2-year-old carriers (R. P. Skoff, unpublished observations). Controls were female littermates (Ta+/ ++, Ta+/Ta+) determined to be noncarriers only after extensive his- tological examination of both optic nerves failed to reveal evidence of mosaicism. In addition, several female offspring from noncarriermoth- ers were used as controls. A total of 25 mice were selected for analysis, 9 14- to 15-d-old mice (6 carriers. 3 normals). 10 30- to 34-d-old mice (4 carriers, 6 normals),- and 6 120- to 170&old mice (3 carriers, 3 normals). Animals were anesthetized with chloral hydrate and sacrificed by intracardiac perfusion using 2% glutaraldehyde and 2% formaldehyde in 0.1 M phosphate buffer. The entire optic nerve and middle cervical segments of the spinal cord were removed, the tissues were osmicated, dehydrated, and embedded in Araldite plastic using routine laboratory procedures. The ventral column of the spinal cord was chosen for analysis because it contains a wide range of different sized fibers and a consistently superior fixation of myelin sheaths was obtained here in comparison to that in the dorsal column. Only the outer half of each ventral column, that portion adjacent to the rim of the ventral fissure, was used in this study (Fig. 1). This same area was reliably located from animal to animal and contained few dendrites that could be confused with unmyelinated axons. Two different morphometric methods were used in this study. A point-counting stereologic method (Williams, 1977) was used to deter- mine the percentage of total area occupied by myelin, the axoplasm of myelinated fibers, and the neuropil in light and electron micrographs. The area occupied by unmyelinated axoplasm was determined on elec- tron micrographs only, which were of sufficient resolution to allow ac- curate identification. Three to 4 photomicrographs, enlarged to x 1800 (encompassing 12,000 pm2 each), and 4-6 electron micrographs, en- larged to x 8500 (encompassing 700 pm2 each), were quantified from each spinal cord. The values derived from these micrographs were summed, and an average for the 4 different parameters measured was calculated for each animal using the Bioquant Point Counting Stereo- logical Package. In addition to point counting, digitization of individual axons and their myelin sheaths was performed on electron micrographs printed at approximately x 15,000. From the spinal cords of the 2-week-old and Figure I. Photomicrograph of the ventral column (PC) adjacent to l-month-old mice, 4-6 micrographs were randomly selected from the the ventral fissure (VI;) in a spinal cord from a 14-d-old normal mouse. same sampling area used for point-counting stereology (Fig. 1). All Dotted line outlines the sampling area from which all light and electron unmyelinated and myelinated axons were digitized in each micrograph. micrographs were taken for morphometric analysis. For each fiber, the perimeter of the axolemma was digitized along with the perimeter of the inner and outer lamellae of the compacted portion “patches” of hypomyelinated fibers were obvious.
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