The extent of liver injury determines hepatocyte fate toward senescence or cancer.

It is well known that induction of hepatocyte senescence could inhibit the development of hepatocellular carcinoma (HCC). Until now, it is still unclear how the degree of liver injury dictates hepatocyte senescence and carcinogenesis. In this study, we investigated whether the severity of injury determines cell fate decisions between hepatocyte senescence and carcinogenesis. After testing of different degrees of liver injury, we found that hepatocyte senescence is strongly induced in the setting of severe acute liver injury. Longer-term, moderate liver injury, on the contrary did not result into hepatocyte senescence, but led to a significant incidence of HCC instead. In addition, carcinogenesis was significantly reduced by the induction of severe acute injury after chronic moderate liver injury. Meanwhile, immune surveillance, especially the activations of macrophages, was activated after re-induction of senescence by severe acute liver injury. We conclude that severe acute liver injury leads to hepatocyte senescence along with activating immune surveillance and a low incidence of HCC, whereas chronic moderate injury allows hepatocytes to proliferate rather than to enter into senescence, and correlates with a high incidence of HCC. This study improves our understanding in hepatocyte cell fate decisions and suggests a potential clinical strategy to induce senescence to treat HCC.

[Cloning of a MADS box protein gene (GhMADS1) from cotton (Gossypium hirsutum L.)].

As a kind of transcription factors, MADS-box protein plays an important role in various cellular processes, especially in the development of floral organs. Based on the contig analysis of the cotton ESTs, the coding region of a cotton MADS-box protein (GhMADS1) was obtained by RT-PCR from floral buds of cotton (G. hirsutum). The cloned fragment of 713 bp (GhMADS1, GenBank accession no. AF538965) contains an open reading frame of 711 bp,coding a polypeptide of 236 amino acids. It was demonstrated that the deduced GhMADS1 protein was highly homologous to the AGL2 group of MADS-box proteins from Vitis vinifera, Nicotiana sylvestris, Petunia hybrida, Arabidopsis thaliana and Antirrhinum majus. Phylogenetic analysis also indicated that GhMADS1 belongs to the AGL2 group of MADS-box proteins. RT-PCR analysis showed that GhMADS1 gene expressed in petals, stamens, ovules and fibers, but not in roots, stems, leaves, bracts and sepals. The strongest expression of GhMADS1 gene was detected in petals. But in floral buds of a cotton homeotic mutant (CHV1), whose floral organs are all converted to bract leaf-like organs, the transcript of GhMADS1 gene was not detected. It was proposed that GhMADS1 gene would be crucial to the development of cotton floral organs.

Analysis of floral morphology of a cotton homeotic variant (CHV1).

Physiological and genetic variations exist frequently in the cotton plants regenerated from somatic embryos. A stable homeotic variant (CHV1) was identified from these regenerated plants. Morphological analysis suggested that all the floral organs of the CHV1 plants convert into bract leaf-like organs, this was confirmed by close inspection of floral organs surface using scanning electron microscope. However, there are placenta and ovules bearing at the basal region of central leaf-like organs. A flower of the variant consists of three to seven bracts, nineteen to fourty one bract leaf-like organs. Arrangement of the leaf-like organs is intermediate between spiral and whorl. The mechanisms responsible for the CHV1 phenotype are analyzed. The variant (CHV1) may be useful in the research of cotton flower development and the mechanism of somaclonal variation.