Genome-Wide Identification and Expression Analysis of the GSK3 Gene Family in Sunflower under Various Abiotic Stresses

Genes in the glycogen synthase kinase 3(GSK3)family are essential in regulating plant response to stressful conditions.This study employed bioinformatics to uncover the GSK3 gene family from the sunflower genome database.The expressions of GSK3 genes in different tissues and stress treatments,such as salt,drought,and cold,were assessed using transcriptome sequencing and quantitative real-time PCR(qRT-PCR).The study results revealed that the 12 GSK3 genes of sunflower,belonging to four classes(Classes I–IV),contained the GSK3 kinase domain and 11–13 exons.The majority of GSK3 genes were highly expressed in the leaf axil and flower,while their expression levels were relatively lower in the leaf.As a result of salt stress,six of the GSK3 genes(HaSK11,HaSK22,HaSK23,HaSK32,HaSK33,and HaSK41)displayed a notable increase in expression,while HaSK14 and HaSK21 experienced a significant decrease.With regard to drought stress,five of the GSK3 genes(HaSK11,HaSK13,HaSK21,HaSK22,and HaSK33)experienced a remarkable rise in expression.When exposed to cold stress,seven of the GSK3 genes(HaSK11,HaSK12,HaSK13,HaSK32,HaSK33,HaSK41,and HaSK42)showed a substantial increase,whereas HaSK21 and HaSK23 had a sharp decline.This research is of great importance in understanding the abiotic resistance mechanism of sunflowers and developing new varieties with improved stress resistance.

Insulin induces PKC-dependent proliferation of mesenteric vascular smooth muscle cells from hypertensive patients

Background and objectives Proliferation of human vascular smooth muscle cells(VSMCs)induced by hyperinsulinemia is a very common clinical pathology.Extensive research has focused on PKC(Protein kinase C)-MAPK(mitogen-activated protein kinase)intracellular signal transduction and the phenotypic modulation accompanied by reorganization of intracellular F-actins in VSMCs.Methods DNA synthesis,signaling of ERK1/2 MAPKs,and changes inα-smooth muscle(SM)actin and F-actin were studied in hypertensive and normotensive human arterial VSMCs exposed to insulin and PMA with and without the PKC inhibitor,GF109203X.Results Differences among cell types in MAPK signaling,α-SM actin,and F-actin isoforms in VSMCs harvested from the arteries of patients with essential hypertension(EH)and normotension(NT)were identified in response to insulin treatment.Proliferation and activation of MAPK were more pronounced in EH VSMCs than in NEH VSMCs.Insulin exposure decreased expression ofα-SM actin and was accompanied by rearrangement of intracellular F-actins in VSMCs,especially in the EH group.These effects were reversed by treatment with the PKC inhibitor.Conclusions Human mesenteric VSMCs of EH and NT patients differed in proliferation,MAPK signaling,and degree of changes inα-SM actin and F-actin isoforms immediately following insulin exposure in vitro.