Store-operated Ca2+ entry (SOCE) represents one of the major Ca2+ entry routes in non-excitable cells. It is involved in a variety of fundamental biological processes and the maintenance of Ca2+ homeostasis. The Ca2+ releaseactivated Ca2+ (CRAC) channel consists of stromal interaction molecule and Orai; however, the role and action of Homer proteins as an adaptor protein to SOCE-mediated Ca2+ signaling through the activation of CRAC channels in non-excitable cells still remain unknown. In the present study, we investigated the role of Homer2 in the process of Ca2+ signaling induced by the interaction between CRACs and Homer2 proteins in non-excitable cells. The response to Ca2+ entry by thapsigargin-mediated Ca2+ store depletion remarkably decreased in pancreatic acinar cells of Homer2–/– mice, as compared to wild-type cells. It also showed critical differences in regulated patterns by the specific blockers of SOCE in pancreatic acinar cells of Homer2–/– mice. The response to Ca2+ entry by the depletion in Ca2+ store markedly increased in the cellular overexpression of Orai1 and STIM1 as compared to the overexpression of Homer2 in cells; however, this response was remarkably inhibited by the overexpression of Orai1, STIM1, and Homer2. These results suggest that Homer2 has a critical role in the regulatory action of SOCE activity and the interactions between CRAC channels.

Under physiological conditions, calcium (Ca2+) regulates essential functions of polarized secretory cells by the stimulation of specific Ca2+ signaling mechanisms, such as increases in intracellular Ca2+ concentration ([Ca2+]i) via the store-operated Ca2+ entry (SOCE) and the receptor-operated Ca2+ entry (ROCE). Homer proteins are scaffold proteins that interact with G protein-coupled receptors, inositol 1,4,5-triphosphate (IP3) receptors, Orai1-stromal interaction molecule 1, and transient receptor potential canonical (TRPC) channels. However, their role in the Ca2+ signaling in exocrine cells remains unknown. In this study, we investigated the role of Homer2 in the Ca2+ signaling and regulatory channels to mediate SOCE and ROCE in pancreatic acinar cells. Deletion of Homer2 (Homer2–/–) markedly increased the expression of TRPC3, TRPC6, and Orai1 in pancreatic acinar cells, whereas these expressions showed no difference in whole brains of wild-type and Homer2–/– mice. Furthermore, the response of Ca2+ entry by carbachol also showed significant changes to the patterns regulated by specific blockers of SOCE and ROCE in pancreatic acinar cells of Homer2–/– mice. Thus, these results suggest that Homer2 plays a critical role in the regulatory action of the [Ca2+]i via SOCE and ROCE in mouse pancreatic acinar cells.

Homer proteins are scaffold proteins that regulate calcium (Ca2+) signaling by modulating the activity of multiple Ca2+ signaling proteins. In our previous report, Homer2 and Homer3 regulated NFATc1 function through its interaction with calcineurin, which then acted to regulate receptor activator of nuclear factor-kappa B ligand (RANKL)-induced osteoclastogenesis and bone metabolism. However, to date, the role of Homers in osteoclastogenesis remains unknown. In this study, we investigated the roles of Homer2 and Homer3 in aging-dependent bone remodeling. Deletion of Homer2 /Homer3 (Homer2/3 DKO) markedly decreased the bone density of the femur. The decrease in bone density was not seen in mice with Homer2 (Homer2−/−) and Homer3 (Homer3−/−) deletion. Moreover, RANKL treatment of bone marrow-derived monocytes/macrophages in Homer2/3 DKO mice significantly increased the formation of multinucleated cells and resorption areas. Finally, Homer2/3 DKO mice decreased bone density in an aging-dependent manner. These findings suggest a novel potent mode of bone homeostasis regulation through osteoclasts differentiation during aging by Homer proteins, specifically Homer2 and Homer3.

소나무재선충병의 방제를 위한 나무주사는 살선충제를 사용하여 예방적인 측면에서 이루어 졌다. 본 연구는 소나무에 살충제를 나무주사하여 약제를 소나무 전체에 침투 이행시킨 후 우화한 매개충이 후식하는 과정에서 약제가 포함된 신초를 섭식하게 되면 소화중독으로 교미 및 산란 전에 살충시킴으로서 매개충을 방제하고자 실시하였 다. 이러한 살충제 나무주사 방법은 신초를 후식하는 하늘소류만을 소화중독에 의해 살충시키는 방법으로 기존의 항공방제에 비해 환경에 대한 영향을 최소화 할 수 있다. 살충제 나무주사에 가장 적합한 약제 선발을 위해 실내에서 Neonicotinoid계 살충제 7종을 각 2,000배로 희석한 후 솔수염하늘소에 2㎕를 경구투입하여 살충효과를 평가한 결과 Clotianidin SL, Thiamethoxam DC이 소화중독에 의한 살충효과가 가장 우수하였으며, 이들 살충제를 야외에서 소나무에 나무주사 후 가지에 망대를 설치하고 솔수염하늘소를 접종하여 살충력을 검정한 결과 Thiamethoxam DC가 살충력이 가장 우수한 것으로 판단되었다. 또한 현장적용을 위해 잣나무림에 나무주사후 산란유인목을 설치하여 무처리구와 비교한 결과 살충제 나무주사 시험지의 산란유인목에서는 산란이 이루어지지 않아 현장방제에 적용 가능성을 확인할 수 있었다.

도시림, 생활림, 가로수, 도시공원 등 국민들의 일상생활을 하는 구역이나 장소에 위치한 생활권 수목 식재지에서의 농약 살포는 농약 살포자의 농약 노출 문제뿐만 아니라 농약의 살포 후 생활권 수목과 접촉하는 불특정 시민들도 지속적인 농약 노출이 문제가 될 수 있다. 본 연구에서는 생활권 수목의 관리를 위해 관행적으로 가장 많이 사용 살포되는 살충제인 Fenitrothion을 회양목에 살포하고 일정시간별로 손 노출량, 잎 잔류량, 호흡 노출량을 측정 한 뒤, 위해성 평가 수식(MOS; margin of safety)을 이용하여 체중별 안전 노출시간을 분석하였다. 그 결과, 살포된 Fenitrothion의 손을 통한 전이량이 급격하게 떨어지고 호흡노출량이 측정되지 않는 48시간 이전 까지는 농약노출에 대한 주의가 필요할 것으로 판단되었다.

The aim of this study was to isolate chicken feather-degrading bacteria with high keratinolytic activity and to investigate cultural conditions affecting keratinolytic enzyme production by a selected isolate. A chicken feather-degrading bacterial strain CH3 was isolated from poultry wastes. Isolate CH3 degraded whole chicken feather completely within 3 days. On the basis of phenotypical and 16S rDNA studies, isolate CH3 was identified as Bacillus thuringiensis CH3. This strain is the first B. thuringiensis described as a feather degrader. The bacterium grew with an optimum at pH 8.0 and 37℃, where maximum keratinolytic activity was also observed. The composition of optimal medium for keratinolytic enzyme production was feather 0.1%, sucrose 0.7%, casein 0.3%, K2HPO4 0.03%, KH2PO4 0.04%, MgCl2 0.01% and NaCl 0.05%, respectively. The keratinolytic enzyme had a pH and temperature optima 9.0 and 45℃, respectively. The keratinolytic activity was inhibited ethylenediaminetetraacetic acid, phenylmethylsulfonyl fluoride, and metal ions like Hg2+, Cu2+ and Zn2+. The enzyme activated by Fe2+, dithiothreitol and 2-mercaptoethanol.