Meloidogyne graminicola has emerged as one of the most destructive plant-parasitic nematodes affecting rice (Oryza sativa) production worldwide.  Resistance to M. graminicola in rice could be the most effective option for its management.  However, sources of germplasm with resistance to M. graminicola in rice remain limited.  Here, we describe the root attraction, gall formation and genetic analysis of the resistance to M. graminicola in the rice variety Huidao 5.  A nematode attraction assay showed that second-stage juveniles (J2s) of M. graminicola were attracted at the root tip of Huaidao 5 within 8 h without a significant reduction in attraction compared to the susceptible rice variety Nanjing 9108.  Microscopic observation of the infection revealed that the J2s invaded root tissues 12 h after inoculation, but their subsequent movement to the root tip was hindered in Huaidao 5, resulting in decreased nematode number compared to Nanjing 9108.  Additionally, we used the soil and hydroponic culture systems to simulate upland and flooding conditions in the paddy fields respectively, and found that gall number was significantly reduced, and nematode development was clearly suppressed in Huaidao 5.  To investigate the genetic basis of this resistance, cross breeding was performed between the Huaidao 5 and Nanjing 9108 varieties.  There was no reduction in the resistance of the F₁ offspring to M. graminicola in the greenhouse or field trials, suggesting that a dominant gene could control resistance in Huaidao 5.  In summary, this study provides a detailed characterization of a novel source of resistance to M. graminicola in rice, which is of great potential for use in crop breeding.

Estrogen plays an important role in regulating testicular Sertoli cell number. Furthermore, S-phase kinase-associated protein 2 (SKP2) plays a central role in mammalian cell cycle progression. The objective of this study was to determine whether 17β-estradiol can regulate the expression of SKP2, and the Sertoli cell cycle, via estrogen receptor β (ERβ), the cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA) and extracellular signal-regulated kinase (ERK1/2) pathway. When cultured immature boar Sertoli cells were treated with 17β-estradiol, a time-dependent increase in SKP2 mRNA and protein level was observed by real-time PCR and Western blot, and 17β-estradiol activity peaked at 30 min. Treatment with ICI182780 and ERβ antagonist reduced 17β-estradiol-induced expression of SKP2 and proliferating cell nuclear antigen (PCNA), while increasing the protein concentration of p27kip1. However, the effect of ERa antagonist on these parameters was lower than that of ICI182780 and ERβ. Forskolin had a similar effect as 17β-estradiol on the expression of SKP2, PCNA and p27kip1. Rp-cAMP, H-89 and U0126 treatment reduced 17β-estradiol-induced changes, while H-89 also inhibited ERK1/2 activation. Therefore, 17β-estradiol mainly regulates SKP2 mRNA and protein expression via ERβ-cAMP-PKA and ERK1/2 activation. SKP2 and PCNA expression were positively correlated, while increased SKP2 expression likely resulted in p27kip1 degradation.