A new dominant mutation which usually manifests itself by causing one or more tail crooks in the heterozygote is described. This mutation, Crooked, symbolCd, arose in strain A. Two inbred albino lines have been established. Line 2159 is normal tailed and in the seventh generation of brother x sister matings. It was selected from Crooked parents which were at F5following outcrossing of a strain A Crooked male to an unrelated black normal tailed female. The Crooked albino line is at F12, since outcrossing to the black female, Prior to this outcross the mutation has been carried for four generations and Was at F86 in strain A. Cd behaves as a partial lethal in the homozygous state. Partial lethality, perhaps better termed partial viability as only 28 % of the homozygotes are born alive, was first inspected from abnormal breeding ratios and later verified by embryological studies. More than 50% of theCd/Od zygotes die before parturition. Exencephaly accounts for another 18% of the homozygotes. Exencephalic embryos have been identified as early as the 11th day of gestation. All exencephalics were alive when observed, but they died Peri-natally. At days 18 and 19 a haemorrhagic amniotic fluid was observed to accompany exencephaly. This haemorrhage is believed to be caused by the rupturing of blood vessels which run laterally along the “bulge”. No spina bifida was observed in the exencephalics. Surviving homozygotes were grossly abnormal. Failure of the lower incisors to erupt is believed to be the primary reason for the SMALLcd/cd mice to lag far behind their litter-mates after 2 weeks of age. In addition to being much smaller than their siblings, these mice have abnormal tail fur and abnormal eyes. Other abnormalities of the SMALL mice which are inconstantly expressed are nervous head movement, kidney absence, bent nose, ‘twisting’, abnormal ear inclination, hydrocephaly and abnormal forelegs, Skeletal studies of the three classes ( + / +,Cd/+ andCd/Cd) showed that specific anomalies are associated with each of these phenotypes. In the hotorozygotes the numerical deficiency of caudal vertebrae is less than one; in the homozygotes it is less than two. Thus, it is evident that the primary effect ofCd is not to cause a marked deficiency of tail vertebrae. The most significant difference between normals and mutants is qualitative. 95 % of the Crookeds have abnormal caudal vertebrae, the normals have none. From a diagnostic standpoint, the best method for distinguishing Cd/+ fromCd/Cd when examining vertebrae, is to inspect the lumbar region: 72% of the homzygotes were abnormal, only 10% of the heterozygotes. A more dependable criterion is found in the skull, where absence of lower incisors and a “pinched” inter-orbital region is indicative of a SMALL phenotype. In conclusion, Cd when homozygous, affects many of the known embryonic systems by disturbing normal organization. Very soon after fertilization approximately one-fourth of the homozygotes are eliminated. During the next 5 clays another one-fourth of the embryos are eliminated and Cd is impressing itself upon all remaining homozygotes as evidenced by later morphological manifestation. As a result of these initiated irregularities there are produced abnormalities of the central nervous system, the most drastic of which results in exencephaly and eliminates another one-fourth of the homozygotes. Nor has Cd completed its effecting of abnormalities by 10 clays. At approximately the 11th day its effects on mesodermal components result in skeletal abnormalities, the most conspicuous of which is Crooked tail. There is no good evidence that Cd causes later developmental changes. The fact that all organogenesis and almost all differentiation of the embryo has been organized by this age would make it likely that the mutant would have completed itsinitiating activity. However, if the formation of the zigzag hairs does not take place until late m the embryo's life, it is possible that Cd remains as a potent disturber of the integumental organization at a late embryonic age. These diverse effects of a single mutant on different embryonic systems make Cd outstandingly different from most of the investigated mouse mutations reported to date. The author is deeply grateful to Prof. L. C. Dunn for advice and helpful discussions throughout the course of this work. To Profs. Landauer, Clark and Dunn the author expresses thanks for critical reading of the original manuscript. For technical assistance with photography the author is indebted to Messrs 0. J. Hodge and F. M. Dillingham.