Canine behavioral genetics — A review

A chronological review of the history of research in canine behavioral genetics is presented. Prior to the work of Scott and Fuller, many studies attempted to describe observed results in simple Mendelian terms. More recently, a quantitative mode of inheritance has been ascribed to many behavioral traits, and heritabilities have been calculated in different populations. Studies of behavioral traits are complicated by the effects of learning, which may well explain the reports of low heritability of behavioral traits measured on adults. Both genotype and environment have been shown to play major roles in the expression of behavioral traits. Maternal effects and the sex of an individual have important effects on behavior scores. Breeders usually select for both physical and behavioral traits in the same individuals, and this review includes a summary of reported research on the relationships between physical and mental traits.     

Genetic code limit organisms — do they exist?

Summary The concept of genetic code limit organisms is introduced. Its DNA composition suggestsTetrahymena pyriformis syngen 1 to be a low G + C coding limit organism. One of the predictions ofTetrahymena's being a coding limit organism—i.e. a particular striking dissimilarity in the composition of the two strands of its DNA duplexes—has been tested experimentally and confirmed.     

Take two people—a genetics teaching kit

This easily made kit has proved very effective in teaching genetics to pupils of low ability     

The genetics of aniridia — simple things become complicated

Aniridia is a rare, panocular disorder characterized by a variable degree of hypoplasia or the absence of iris tissue associated with additional ocular abnormalities. It is inherited in an autosomal dominant manner, with high penetrance and variable expression even within the same family. In most cases the disease is caused by haploinsufficiency truncating mutations in the PAX6 gene; however, in up to 30% of aniridia patients, disease results from chromosomal rearrangements at the 11p13 region. The aim of this review is to present the clinical and genetic aspects of the disease. Furthermore, we present a molecular diagnostic strategy in the aniridia patients. Recent improvement in the genetic diagnostic approach will precisely diagnosis aniridia patients, which is essential especially for children with aniridia in order to determine the risk of developing a Wilms tumor or neurodevelopmental disorder. Finally, based on the previous studies we describe the current knowledge and latest research findings in the topic of pathogenesis of aniridia and possible future treatment.     

Rye cytology,cytogenetics and genetics — current status

Summary Progress in rye karyology is reviewed with respect to chromosome structure, recognition and chromosome nomenclature. Considerable contributions have been brought about by molecular techniques which have even revealed nucleotide sequences of some of the ribosomal DNA. DNA sequence organization correlates with the distribution of major Giemsa C-band regions as well as with N-bands and the binding sites of fluorescent dyes. The several banding patterns permit the classification of rye chromosomes. The increased data and widespread application of banding analysis require a consistent system of chromosome and/or band designation. Therefore, a standard band nomenclature is proposed with reference to the recommendations of the Paris Conference on Standardization in Human Cytogenetics. In addition, advances in genetics are summarized and discussed. Based on the original accepted standard karyogram and banding patterns of the rye chromosomes, meanwhile, 120 genes determining several characters have been associated with individual chromosomes and/or chromosome arms, including linkage studies for about 19 arrangements. Most results were obtained using wheat-rye addition lines as well as test crosses with defined translocations. Moreover, genetical studies based on appropriate trisomic and telotrisomic material resulted in the localization of 19 genes, including their linkage relationships.     

Statistical properties of polymorphism in host—parasite genetics

Summary Host—parasite interactions often have complex dynamics. At the level of individual allele frequencies, the dynamics are difficult to predict and difficult to measure. However, aggregate properties of polymorphism, such as allelic diversity or the frequency of resistance, may be relatively easy to work with. I study this problem with computer simulations of a host—parasite model. In one example, the simulations show that the allelic diversity at a locus is similar in a host—parasite model and a neutral model in which drift is the only evolutionary process. Allelic diversity is similar in the two models, even though the temporal dynamics of individual allele frequencies are very different. In a second example, the genetic system that would be inferred from analysing samples of hosts and parasites is quite different from the actual specificity that determines the dynamics of the system. Thus, general conclusions about the specificity of host—parasite genetics must be analysed in the context of the expected statistical distributions of polymorphism. The final example shows that the frequency of resistance provides an interesting aggregate measure of host—parasite polymorphism. If the ratio of parasite generation time to the time between the reproductive seasons of the hosts is small, then no regular periodicity in the frequency of resistance occurs. However, if parasites have many generations per reproductive season of the host, then resistance fluctuates with a period equal to the seasonality of the host. The important role of seasonality shown here differs from the emphasis in previous theories on the relative generation times of host and parasite.     

Molecular genetics of the NCLs — status and perspectives

The neuronal ceroid lipofuscinoses (NCLs) are a group of inherited neurodegenerative disorders characterized by the accumulation of autofluorescent storage material in many cell types, including neurons. Most NCL subtypes are inherited in an autosomal recessive manner and characterized clinically by epileptic seizures, progressive psychomotor decline, visual failure, variable age of onset, and premature death. To date, seven genes underlying human NCLs have been identified. Most of the mutations in these genes are associated with specific disease subtypes, while some result in variable disease onset, severity and progression. In addition to these, there are still disease subgroups with unknown molecular genetic backgrounds. Although apparent clinical homogeneity exists within some of these subgroups, actual genetic heterogeneity may complicate gene identification. Additional clues to the identification of these unknown genes may come from animal models of NCL and from functional studies of already known genes which may suggest further candidates.