Chemical compositions and biological activities of essential oil leaves cultivated in Vietnam (Thua Thien Hue).

is an evergreen citrus plant and has attracted considerable attention due to its bioactive components and biological activities. In the present study, the essential oil (EO) from cultivated in Vietnam was demonstrated to exhibit the in vitro antioxidant, thrombolytic, anti-hemolysis, anti-inflammatory, and antidiabetic activities. Briefly, the gas chromatography coupled to mass spectrometry analysis revealed that the leaf EO of was composed of 33 components, with the main constituents being β-carypphyllene (32.

Two-step imprinted X inactivation: repeat versus genic silencing in the mouse.

Mammals compensate for unequal X-linked gene dosages between the sexes by inactivating one X chromosome in the female. In marsupials and in the early mouse embryo, X chromosome inactivation (XCI) is imprinted to occur selectively on the paternal X chromosome (X(P)). The mechanisms and events underlying X(P) imprinting remain unclear.

Perinucleolar targeting of the inactive X during S phase: evidence for a role in the maintenance of silencing.

In mammalian females, two X chromosomes are epigenetically distinguished as active and inactive chromosomes to balance X-linked gene dosages between males and females. How the Xs are maintained differently in the same nucleus remains unknown. Here, we demonstrate that the inactive X (Xi) is targeted to a distinct nuclear compartment following pairing with its homologous partner.

Epigenetic dynamics of the Kcnq1 imprinted domain in the early embryo.

The mouse Kcnq1 imprinted domain is located on distal chromosome 7 and contains several imprinted genes that are paternally repressed. Repression of these genes is regulated by a non-coding antisense transcript, Kcnq1ot1, which is paternally expressed. Maternal repression of Kcnq1ot1 is controlled by DNA methylation originating in the oocyte.

Differential methylation of Xite and CTCF sites in Tsix mirrors the pattern of X-inactivation choice in mice.

During mammalian dosage compensation, one of two X-chromosomes in female cells is inactivated. The choice of which X is silenced can be imprinted or stochastic. Although genetic loci influencing the choice decision have been identified, the primary marks for imprinting and random selection remain undefined.

X-chromosome inactivation: a hypothesis linking ontogeny and phylogeny.

In mammals, sex is determined by differential inheritance of a pair of dimorphic chromosomes: the gene-rich X chromosome and the gene-poor Y chromosome. To balance the unequal X-chromosome dosage between the XX female and XY male, mammals have adopted a unique form of dosage compensation in which one of the two X chromosomes is inactivated in the female. This mechanism involves a complex, highly coordinated sequence of events and is a very different strategy from those used by other organisms, such as the fruitfly and the worm.

Inheritance of a pre-inactivated paternal X chromosome in early mouse embryos.

In mammals, dosage compensation ensures equal X-chromosome expression between males (XY) and females (XX) by transcriptionally silencing one X chromosome in XX embryos. In the prevailing view, the XX zygote inherits two active X chromosomes, one each from the mother and father, and X inactivation does not occur until after implantation. Here, we report evidence to the contrary in mice.

CTCF, a candidate trans-acting factor for X-inactivation choice.

In mammals, X-inactivation silences one of two female X chromosomes. Silencing depends on the noncoding gene, Xist (inactive X-specific transcript), and is blocked by the antisense gene, Tsix. Deleting the choice/imprinting center in Tsix affects X-chromosome selection.