Phagocytosis of invading microbes requires dynamic rearrangement of the plasma membrane and its associated cytoskeletal actin network. The polarization of Cdc42 and Rac1 Rho GTPases to the site of plasma membrane protrusion is responsible for the remodeling of actin structures. However, the mechanism of Rho GTPase recruitment to these sites and the identities of accessory molecules involved in this process are not well understood. In this study, we uncovered several new components involved in innate immunity in Drosophila melanogaster. Our data demonstrate that Rab35 is a regulator of vesicle transport required specifically for phagocytosis. Moreover, recruitment of Cdc42 and Rac1 to the sites of filopodium and lamellipodium formation is Rab35 dependent and occurs by way of microtubule tracks. These results implicate Rab35 as the immune cell-specific regulator of vesicle transport within the actin-remodeling complex.

본 연구에서는 GFRP 하부근과 상부근의 정착길이 설계식을 제안하기 위하여 실험적 연구를 수행하고 실험결과의 통계적 분석을 실시하였다. 상부근과 하부근 각각 52개의 수정인발실험을 계획하였으며, 실험변수는 보강근의 묻힘길이(보강근 지름의 15, 30, 45배), 순피복두께(보강근 지름의 0.5-2.0배), 상부근 효과, 보강근 종류(국내산 2종, 국외산 1종 등 3종) 및 보강근지름(D10, D13, D16)이다. 하부근과 하부근 각각에 대하여 수정인발실험을 통하여 평균부착강도를 결정하고, 평균부착강도에 대한 2변수 선형회귀분석을 실시하였다. 2변수 선형 회귀분석의 결과에 대하여 5% 분위수를 적용하여 보수적인 방법으로 정착길이 설계식을 제안하였다. 2변수 선형 회귀분석에 의한 하부근과 하부근의 정착길이 설계식을 제안하고 상부근과 하부근의 정착식을 비교하고, ACI 440.1R-06 식과 비교하였다. The objective of this study was to propose a development length equation for bottom and top GFRP bars. Including the bottom and top GRPP bars, a total of 104 modified pullout tests were completed. The test variables were embedment length (15, 30, 45db), net cover thickness (0.5~2.0db), different GFRP bar types, and bar diameters (10, 13, 16mm). The average bond stresses were determined based on the modified pullout test results. Two variable linear regression analyses were performed on the results of the average bond stresses. Utilizing the 5% fractile concept, a conservative development length design equation was derived. The design equation of the development length for bottom and top GFRP bars was proposed and the design equation derived in this study was compared to the ACI 440.1R-06 committee equation.

Essential aspects of the innate immune response to microbial infection appear to be conserved between insects and mammals. Although signaling pathways that activate NF-kappa B during innate immune responses to various microorganisms have been studied in detail, regulatory mechanisms that control other immune responses to fungal infection require further investigation. To identify new Drosophila genes involved in antifungal immune responses, we selected genes known to be differentially regulated in SL2 cells by microbial cell wall components and tested their roles in antifungal defense using mutant flies. From 130 mutant lines, sixteen mutants exhibited increased sensitivity to fungal infection. Examination of their effects on defense against various types of bacteria and fungi revealed nine genes that are involved specifically in defense against fungal infection. All of these mutants displayed defects in phagocytosis or activation of antimicrobial peptide genes following infection. In some mutants, these immune deficiencies were attributed to defects in hemocyte development and differentiation, while other mutants showed specific defects in immune signaling required for humoral or cellular immune responses. Our results identify a new class of genes involved in antifungal immune responses in Drosophila.

IκB kinase (IKK) and Jun N-terminal kinase (Jnk) signaling modules are important in the synthesis of immune effector molecules during innate immune responses against lipopolysaccharide and peptidoglycan. However, the regulatory mechanisms required for specificity and termination of these immune responses are unclear. We show here that crosstalk occurred between the drosophila Jnk and IKK pathways, which led to downregulation of each other's activity. The inhibitory action of Jnk was mediated by binding of drosophila activator protein 1 (AP1) to promoters activated by the transcription factor NF-κB. This binding led to recruitment of the histone deacetylase dHDAC1 to the promoter of the gene encoding the antibacterial protein Attacin-A and to local modification of histone acetylation content. Thus, AP1 acts as a repressor by recruiting the deacetylase complex to terminate activation of a group of NF-κB target genes.