SIMULTANEOUS OVER-EXPRESSION OF INSULIN-LIKE GROWTH FACTOR- Ⅱ (IGF- Ⅱ ) AND IGF- Ⅱ RECEPTOR(IGF- Ⅱ R) GENES IN HUMAN PRIMARY CANCER-IMPLICATION OF AUTOCRINE AND PARACRINE MECHANISM IN AUTONOMOUS GROWTH OF HEPATIC CANCER

This is first report about the simultaneous over-expression of both Insulin-like growth factor (IGF- I ) and its receptor (IGF- I R) at mRNA level in human primary hepatic Cancer (PHC). In 10 PHC samples from China, IGF-I and IGF- I R were both over-expressed, whereas only a background signal was detected in normal liver. In 5 pairs of PHC and its non- tumorous adjacent liver tissues from South Africa, IGF- I and IGF- I R were also over-expressed in PHC. mRNA expression of IGF- I in all 5 cases and IGF- I R in 4 of 5 cases were higher in cancer than non- tumorous adjacent liver tissues. These results strongly implicate that an autocrine and/ or paracrine mechanism might be Involved in formation and progression of PHC.

Combining single-cell RNA sequencing with spatial transcriptome analysis reveals dynamic molecular maps of cambium differentiation in the primary and secondary growth of trees

Primary and secondary growth of the tree stem are responsible for corresponding increases in trunk height and diameter.However,our molecular understanding of the biological processes that underlie these two types of growth is incomplete.In this study,we used single-cell RNA sequencing and spatial transcriptome sequencing to reveal the transcriptional landscapes of primary and secondary growth tissues in the Populus stem.Comparison between the cell atlas and differentiation trajectory of primary and secondary growth revealed different regulatory networks involved in cell differentiation from cambium to xylem precursors and phloem precursors.These regulatory networks may be controlled by auxin accumulation and distribution.Analysis of cell differentiation trajectories suggested that vessel and fiber development followed a sequential pattern of progressive transcriptional regulation.This research provides new insights into the processes of cell identity and differentiation that occur throughout primary and secondary growth of tree stems,increasing our understanding of the cellular differentiation dynamics that occur during stemgrowth in trees.

BAK1 plays contrasting roles in regulating abscisic acid-induced stomatal closure and abscisic acid-inhibited primary root growth in Arabidopsis

The mechanisms that balance plant growth and stress responses are poorly understood, but they appear to involve abscisic acid(ABA) signaling mediated by protein kinases. Here, to explore these mechanisms, we examined the responses of Arabidopsis thaliana protein kinase mutants to ABA treatment. We found that mutants of BRASSINOSTEROID INSENSITIVE 1-ASSOCIATED RECEPTOR KINASE 1(BAK1) were hypersensitive to the effects of ABA on both seed germination and primary root growth. The kinase OPEN STOMATA 1(OST1) was more highly activated by ABA in bak1 mutant than the wild type. BAK1 was not activated by ABA treatment in the dominant negative mutant abi1-1 or the pyr1 pyl4 pyl5 pyl8 quadruple mutant, but it was more highly activated by this treatment in the abi1-2 abi2-2 hab1-1 loss-of-function triple mutant than the wild type. BAK1 phosphorylates OST1 T146 and inhibits its activity. Genetic analyses suggested that BAK1 acts at or upstream of core components in the ABA signaling pathway, including PYLs, PP2 Cs,and Sn RK2 s, during seed germination and primary root growth. Although the upstream brassinosteroid(BR) signaling components BAK1 and BR INSENSITIVE 1(BRI1) positively regulate ABAinduced stomatal closure, mutations affecting downstream components of BR signaling, including BRASSINOSTEROID-SIGNALING KINASEs(BSKs)and BRASSINOSTEROID-INSENSITIVE 2(BIN2), did not affect ABA-mediated stomatal movement. Thus,our study uncovered an important role of BAK1 in negatively regulating ABA signaling during seed germination and primary root growth, but positively modulating ABA-induced stomatal closure, thus optimizing the plant growth under drought stress.