The E3 ubiquitin ligase RING1 interacts with COP9 Signalosome Subunit 4 to positively regulate resistance to root-knot nematodes in Solanum lycopersicum L.

Globally, root-knot nematodes (RKNs) cause massive production losses in all major crops. E3 ubiquitin ligases are involved in plant growth, development and immune response. But their roles in plant defense against RKNs are largely unclear. Here, we show that tomato E3 ubiquitin ligase RING1 interacts with COP9 Signalosome Subunit 4 (CSN4) which is essential for jasmonic acid (JA)-dependent basal defense against RKNs. Tissue-specific expression analysis showed that RING1 expression was the highest in tomato roots and the expression was significantly increased with RKN (Meloidogyne incognita) infection. Compared with the wild-type plants, the number of egg masses in roots significantly increased in the ring1 mutants, while RING1 overexpression conferred resistance against RKNs. Furthermore, RKN infection increased the accumulation of CSN4 protein in the roots of wild-type plants, which was largely compromised in the ring1 mutants but was enhanced in the RING1 overexpressing plants. The RKN-induced transcripts of JA biosynthetic and signaling genes as well as the accumulation of JA and JA-isoleucine were compromised in ring1 mutants but were increased in RING1 overexpressing plants. These results suggest that RING1 positively regulates JA-dependent basal defense against RKNs by interacting with CSN4 proteins.

[Association between clinical ischemic events and carotid calcification evaluated by 64 slices CT angiography].

OBJECTIVE: To explore the relationship between clinical ischemic events and carotid calcification detected by 64 slices CT angiography. METHODS: We retrospectively analyzed the carotid calcified plaques in 116 patients underwent the 64 slices CT angiography. The relationship between the carotid calcification and the clinical ischemic events was analyzed. RESULTS: A total of 377 plaques were detected and the incidence of carotid plaque calcification was 63.40%. Incidence of plaque calcification was significantly lower in patients with ages < 50 years than that in patients with ages 51 - 59 years, 60 - 69 years and higher than 70 years (P = 0.003, P = 0.002, P = 0.000, respectively). The incidence of plaque calcification in the common carotid artery was significantly lower than the carotid bifurcation (P = 0.000) and the internal carotid artery (P = 0.000). The incidences of calcification in the mild, moderate and severe degree of stenosis and occlusion were 46.54%, 33.33%, 26.67% and 0% respectively. The distribution of intraplaque calcium was similar between patients with ischemic event and non-ischemic event group. However, the incidence of calcification was significantly lower patients with ischemic event than that in patients without ischemic event (30.34% vs. 43.10%, P = 0.013). Calcified plaque was negatively associated with ischemic event (beta = -0.688, P = 0.006). CONCLUSION: 64 slices CT angiography can analyze the characterization of carotid plaque calcium.