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Phosphine resistance in stored-product insects occurs worldwide and is a major challenge to continued effective use of this fumigant. We determined resistance frequencies and levels of resistance in Tribolium castaneum and Plodia interpunctella collected from California almond storage and processing facilities. Discriminating doses of phosphine were established for eggs and larvae of P. interpunctella and eggs of T. castaneum using laboratory susceptible strains of the two species. For T. castaneum and P. interpunctella eggs, discriminating doses were 62.4 and 107.8 ppm, respectively, over a 3-d fumigation period, and for P. interpunctella larvae, discriminating dose was 98.7ppm over a 20-h fumigation period. Discriminating dose tests on adults and eggs showed that 4 out of 11 T. castaneum populations tested had resistance frequencies that ranged from 42 to 100% for adults and 54 to 100% for eggs. LC99 values for the susceptible and the most resistant adults of T. castaneum were 7.4 and 356.9 ppm over 3 d, respectively. LC99 values for T. castaneum eggs were 51.5 and 653.9 ppm, respectively. Based on adult data, the most resistant T. castaneum beetle population was 49× more resistant than the susceptible strain. Phosphine resistance frequencies in P. interpunctella eggs ranged from 4 to 20%. Results show phosphine resistance is present in both species in California. Future research will investigate phosphine resistance over a wider geographic area. In addition, the history of pest management practices in facilities where insects tested in this study originated will be determined in order to develop phosphine resistance management strategies for California almond storage and processing facilities. [ABSTRACT FROM AUTHOR]

Here we describe methods for (a) collecting starfish during their breeding period; (b) maintaining adults with fully grown gonads in laboratory aquaria; (c) rearing fertilized eggs to brachiolaria larvae, and (d) inducing larvae to metamorphose into juveniles under laboratory conditions. Such protocols should facilitate various analyses of starfish development throughout the entire life cycle of these model organisms.

The Japanese government is making full-scale efforts to support working people who suffer from cancer and/or other diseases, as it seeks to support a balance of work and receiving medical treatment. The Hospital of the University of Occupational and Environmental Health, Japan, opened its Support Center of Treatment and Work Balance in 2018. This is a multi-disciplinary department for supporting the balance of work and medical treatment. It also opened its Department of Occupational Medicine, the first such department in Japan to provide medical diagnosis and treatment dedicated to supporting that same balance. Our team has supported 704 patients through our activities over the past 3 years. The number of patients supported has increased each year, while the number of departments providing support has also trended upward. There has also been an increase in opinions by attending physicians regarding employment, as well as the number of cases covered by public medical insurance. Here we suggest two factors in our hospital's growth in these activities: (1) many of the clinicians are qualified as occupational physicians, and (2) the organizational strength of our team, which has a vision for balancing support and subsequently promotes that vision. We hope that this report will lead to the balance of support activities in Japan and contribute to the model internationally.

Oocyte maturation is a process wherein an oocyte arrested at prophase of meiosis I resumes meiosis to become a fertilizable egg. In starfish ovaries, a hormone released from follicle cells activates the oocytes, resulting in an increase in their intracellular pH (pH i ), which is required for spindle assembly. Herein, we describe a protocol for pH i measurement in living oocytes microinjected with the pH-sensitive dye BCECF. For in vivo BCECF calibration, we treated oocytes with artificial seawater containing CH 3 COONH 4 to clamp pH i , injected pH-standard solutions, and converted the BCECF fluorescence intensity ratios to pH i values. Of note, if the actual pH i is higher or lower than the known pH of injected standard solutions, the BCECF fluorescence intensity ratio will decrease or increase, respectively. On the other hand, the pH of the injected solution displaying no change in fluorescence intensity should be considered the actual pH i . These methods for pH i calibration and clamping are simple and reproducible., Competing Interests: Competing interestsThe authors declare no competing financial interests., (Copyright © 2020 The Authors; exclusive licensee Bio-protocol LLC.)

Tight regulation of intracellular pH (pH i ) is essential for biological processes. Fully grown oocytes, having a large nucleus called the germinal vesicle, arrest at meiotic prophase I. Upon hormonal stimulus, oocytes resume meiosis to become fertilizable. At this time, the pH i increases via Na + /H + exchanger activity, although the regulation and function of this change remain obscure. Here, we show that in starfish oocytes, serum- and glucocorticoid-regulated kinase (SGK) is activated via PI3K/TORC2/PDK1 signaling after hormonal stimulus and that SGK is required for this pH i increase and cyclin B-Cdk1 activation. When we clamped the pH i at 6.7, corresponding to the pH i of unstimulated ovarian oocytes, hormonal stimulation induced cyclin B-Cdk1 activation; thereafter, oocytes failed in actin-dependent chromosome transport and spindle assembly after germinal vesicle breakdown. Thus, this SGK-dependent pH i increase is likely a prerequisite for these events in ovarian oocytes. We propose a model that SGK drives meiotic resumption via concomitant regulation of the pH i and cell cycle machinery., (© 2019 Hosoda et al.)

The kinase cyclin B-Cdk1 complex is a master regulator of M-phase in both mitosis and meiosis. At the G2/M transition, cyclin B-Cdk1 activation is initiated by a trigger that reverses the balance of activities between Cdc25 and Wee1/Myt1 and is further accelerated by autoregulatory loops. In somatic cell mitosis, this trigger was recently proposed to be the cyclin A-Cdk1/Plk1 axis. However, in the oocyte meiotic G2/M transition, in which hormonal stimuli induce cyclin B-Cdk1 activation, cyclin A-Cdk1 is nonessential and hence the trigger remains elusive. Here, we show that SGK directly phosphorylates Cdc25 and Myt1 to trigger cyclin B-Cdk1 activation in starfish oocytes. Upon hormonal stimulation of the meiotic G2/M transition, SGK is activated by cooperation between the Gβγ-PI3K pathway and an unidentified pathway downstream of Gβγ, called the atypical Gβγ pathway. These findings identify the trigger in oocyte meiosis and provide insights into the role and activation of SGK., (© 2019 Hiraoka et al.)

A 35-kDa protein, ANA, belongs to an emerging family of antiproliferative proteins consisting of Tob, Tob2, ANA / BTG3, PC3B, PC3 / TIS21 / BTG2, and BTG1. All of these, except ANA and PC3B, have been shown to interact with the CCR4 transcription factor-associated protein Caf1. Here we show that ANA also associates with Caf1, ANA being the preferred partner of Caf1 among the Tob family proteins. Although ANA is likely to interact with Caf1 at its amino-terminal half, which is conserved among the family members, our data suggest that the carboxyl-terminal half of ANA plays a role in the interaction. Finally, in situ hybridization experiments revealed that expression of Caf1 overlaps at least in part with that of ANA. Thus, ANA could function through its interaction with Caf1.

Bone morphogenetic protein (BMP) controls osteoblast proliferation and differentiation through Smad proteins. Here we show that Tob, a member of the emerging family of antiproliferative proteins, is a negative regulator of BMP/Smad signaling in osteoblasts. Mice carrying a targeted deletion of the tob gene have a greater bone mass resulting from increased numbers of osteoblasts. Orthotopic bone formation in response to BMP2 is elevated in tob-deficient mice. Overproduction of Tob represses BMP2-induced, Smad-mediated transcriptional activation. Finally, Tob associates with receptor-regulated Smads (Smad1, 5, and 8) and colocalizes with these Smads in the nuclear bodies upon BMP2 stimulation. The results indicate that Tob negatively regulates osteoblast proliferation and differentiation by suppressing the activity of the receptor-regulated Smad proteins.