Summary• Root-knot nematodes (RKNs) are obligate endoparasites that maintain a biotrophic relationship with their hosts over a period of several weeks and induce the differentiation of root cells into specialized feeding cells. Nematode effectors synthesized in the oesophageal glands and injected into the plant tissue through the syringe-like stylet certainly play a central role in these processes.• In a search for nematode effectors, we used comparative genomics on expressed sequence tag (EST) datasets to identify Meloidogyne incognita genes encoding proteins potentially secreted upon the early steps of infection.• We identified three genes specifically expressed in the oesophageal glands of parasitic juveniles that encode predicted secreted proteins. One of these genes, Mi-EFF1 is a pioneer gene that has no similarity in databases and a predicted nuclear localization signal. We demonstrate that RKNs secrete Mi-EFF1 within the feeding site and show Mi-EFF1 targeting to the nuclei of the feeding cells.• RKNs were previously shown to secrete proteins in the apoplasm of infected tissues. Our results show that nematodes sedentarily established at the feeding site also deliver proteins within plant cells through their stylet. The protein Mi-EFF1 injected within the feeding cells is targeted at the nuclei where it may manipulate nuclear functions of the host cell.

The negative correlation between cb free BPA and INSL3 provides indirect evidence for an impact of EEDs on human fetal Leydig cell INSL3 production and points to cbINSL3 as a possible target of EED action during fetal testis development.

SummaryBackground Cryptorchidism, the most frequent congenital malformation in full-term male newborns, increases the risk of hypofertility and testicular cancer. Most cases remain idiopathic but epidemiological and experimental studies have suggested a role of both genetic and environmental factors. Physiological testicular descent is regulated by two major Leydig hormones: insulin-like peptide 3 (INSL3) and testosterone. Objectives To study the endocrine context at birth as a reflection of late pregnancy in isolated idiopathic cryptorchidism and to analyse the possible disruptions of INSL3 and/or testosterone. Methods From a prospective case-control study at Nice University Hospital, we assessed 180 boys born after 34 weeks gestation: 52 cryptorchid (48 unilateral, 4 bilateral; 26 transient, 26 persistent), and 128 controls matched for term, weight and time of birth. INSL3 and testosterone were measured in cord blood and compared in both groups as were other components of the pituitary-gonadic axis: LH, HCG, FSH, AMH and SHBG. Results INSL3 was decreased in cryptorchid boys (P = 0Á031), especially transient cryptorchid (P = 0Á029), while testosterone was unchanged as were the other hormones measured. INSL3 was significantly decreased (P = 0Á018) in the group of 20 with nonpalpable testes compared with the group of 21 with palpable testes (15 suprascrotal, five inguinal, one high scrotal) according to Scorer classification. In the whole population, INSL3 correlated positively with LH and negatively with AMH, but with no other measured hormones. Conclusions INSL3 but not testosterone is decreased at birth in idiopathic cryptorchidism, especially in transient forms. This hormonal decrease may contribute to the impaired testicular

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