Genetic imprinting

Content
Sex Determination, Sex Differentiation, Dosage Compensation and Genetic Imprinting
Chromosome Theory of Sex Determination 
Balance Theory of Sex Determination X/A ratio in Drosophila
Triploid intersexes in Drosophila and genie balance theory
X/A ratio and gynandromorphs in Drosophila
X/A ratio in Coenorhabditis elegans (a free living nematode)
Balance Between Male and Female Factors
- Diploid intersexes in gypsy moth (Lymantria)
- X/A ratio and multiple numerator elements (Drosophila and Coenorhabditis)
Sex Determination in Plants
Methods for determining heterogametic sex in plants
Sex determination in Coccinia and Melandrium
Sex determination in other dioecious plants
Sex Chromosomes in Mammals Including Humans (Homo sapiens)
TDF, ZFY and SRY genes in humans
H-Y antigen and male development in mammals
Single gene control of sex
Sex determination in Asparagus
Tassel seed (ts) and silkless (sk) genes in maize
Transformer gene (tra)in Drosophila
Haploid males in Hymenoptera
Hormonal control of sex
Environmental Sex Determination in Reptiles
Dosage Compensation in Organisms with Heterogametic Males
X-chromosome inactivation in mammals
Position effect variegation
Hyperactivity of X-chromosome in male Drosophila
Lack of Dosage Compensation in Organisms with Heterogametic Females
Genetic imprinting


Genetic imprinting is a phenomenon, which involves differences in expression of genes inherited from mother and father. In other words, the chromosomes in the sperm and egg are differentially imprinted or marked as having come from the father or the mother, so that some maternally inherited genes and other paternally inherited genes are differentially expressed in the progeny.

Any epigenetic changes in the germ cells, such as the inactivation of an X-chromosome, are reversed or altered during or just before meiosis, which leads to the production of sperms and eggs. After this reversal of epigenetic changes, the eggs and sperms are differentially imprinted. As a consequence of this, even if a chromosome in a sperm happens to have been inherited from the fathers’ mother, it would still bear the male imprint (Fig. 17.24). Such imprinting has been found to be crucial to normal development in mice and other mammals, because it silences and activates different sets of genes in the maternal and paternal chromosomes. These differences in paternal and maternal chromosomes complement each other in directing normal development. This differentiation or reprogramming of the genome is believed to be achieved through changes in methylation patterns. In mice, differential methylation of paternal and maternal chromosomes has actually been demonstrated.

A case of genetic imprinting has also been shown in human patients suffering with a disease known as Beckwith Wiedermann Syndrome (BWS), where both copies of a region on the short arm of chromosome 11 (Up 15.5)were inherited from the father. This feature is described as paternal disomy. A similar situation has been shown involving paternal disomy for mouse chromosome 7 (homologous to human chromosome 11), which led to production of abnormally large embryos, a condition analogous to BWS in humans. This is attributed to differential paternal expression (imprinting) of a gene Igf2(insulin like growth factor-2) in mouse, which is believed to be homologous to BWS-gene in humans.
 
Genetic imprinting of chromosomes, so that they are identifiable as having been donated to an individual (a) by its father (dotted screen) or (b) by its mother (solid black). This imprinting may persist for many cell generations, but disappears in germ cells during meiosis.
Fig. 17.24. Genetic imprinting of chromosomes, so that they are identifiable as having been donated to an individual (a) by its father (dotted screen) or (b) by its mother (solid black). This imprinting may persist for many cell generations, but disappears in germ cells during meiosis.