Application of prohexadione-calcium priming affects Brassica napus L. seedlings by regulating morph-physiological characteristics under salt stress.

Salinity stress imposes severe constraints on plant growth and development. Here, we explored the impacts of prohexadione-calcium (Pro-Ca) on rapeseed growth under salt stress. We designed a randomized block design pot experiment using two rapeseed varieties, 'Huayouza 158R' and 'Huayouza 62'. We conducted six treatments, S0: non-primed + 0 mM NaCl, Pro-Ca+S0: Pro-Ca primed + 0 mM NaCl, S100: non-primed + 100 mM NaCl, Pro-Ca+S100: Pro-Ca primed + 100 mM NaCl, S150: non-primed + 150 mM NaCl, Pro-Ca+S150: Pro-Ca primed + 150 mM NaCl. The morphophysiological characteristics, and osmoregulatory and antioxidant activities were compared for primed and non-primed varieties. Our data analysis showed that salt stress induced morph-physiological traits and significantly reduced the antioxidant enzyme activities in both rapeseed varieties. The Pro-Ca primed treatment significantly improved seedlings, root, and shoot morphological traits and accumulated more dry matter biomass under salt stress. Compared to Huayouza 158R, Huayouza 62 performed better with the Pro-Ca primed treatment. The Pro-Ca primed treatment significantly enhanced chlorophyll content, net photosynthetic rate (Pn), stomatal conductance (Gs), transpiration rate (Tr), and actual photochemical quantum efficiency (ФPSII). Furthermore, the Pro-Ca primed treatment also improved ascorbic acid (ASA) content, superoxide dismutase (SOD), peroxidase (POD), catalase (CAT), and ascorbate peroxidase (APX) activity, and stimulated the accumulation of soluble proteins. These findings strongly suggested that the Pro-Ca primed treatment may effectively counteract the negative impacts of salinity stress by regulating the morph-physiological and antioxidant traits.

Midbody remnant regulates the formation of primary cilia and their roles in tumor growth. / ä¸­é—´ä½“æ®‹ä½“ä¸Žåˆçº§çº¤æ¯›çš„å ³ç³»åŠå ¶åœ¨è‚¿ç˜¤ç”Ÿé•¿ä¸­çš„ä½œç”¨.

Recent studies have shown that the formation of the primary cilium is associated with a specific cellular organelle known as the midbody remnant (MBR), which is a point-like organelle formed by shedding of the midbody at the end of mitosis. MBRs move along the cell surface close to the center body and regulate it to form primary cilia at the top of the centriole. Primary cilia can act as an organelle to inhibit tumorigenesis, and it is lost in a variety of tumors. Studies have shown that the accumulation of MBRs in tumor cells affects ciliogenesis; in addition, both MBRs and primary cilia are degraded in tumor cells through the autophagy pathway, and MBRs can also transfer tumor signaling pathway factors to primary cilia affecting tumorigenesis. In this article, the basic structure and the formation process of MBR and primary cilia are reviewed and the mechanism of MBRs regulating ciliogenesis is elaborated. The significance of MBR-mediated ciliogenesis in tumorigenesis and its potential as a target for cancer treatment are discussed.

SHCBP1 Overexpression Aggravates Pancreatitis by Triggering the Loss of Primary Cilia.

Primary cilia are microtubule-based organelles that mediate various biological processes. Pancreatic cells are typically ciliated; however, the role of primary cilia in acute pancreatitis (AP) is largely unknown. Here, we report that the loss of primary cilia, mediated by SHCBP1 (SHC1 binding protein), exerted a provocative effect on AP. Primary cilia are extensively lost in inflamed pancreatic cells in vitro and in mouse tissues with AP in vivo. Abrogation of primary cilia aggravated lipopolysaccharide (LPS)-induced inflammation in pancreatic cells. Mechanistically, AP induced the overexpression of SHCBP1 mitotic factor, which is localized to the base of primary cilia. SHCBP1 deficiency relieved LPS- and cerulein-induced pancreatitis by preventing the loss of primary cilia in vitro and in vivo. Collectively, we reveal that inflammation-induced loss of primary cilia aggravates AP. Furthermore, abrogating SHCBP1 to prevent primary cilia loss is an efficient strategy to combat AP.