根据巴恩大学的研究人员发表于PNAS的研究指出，发光杆菌会制造一种抗生素，抑制一种昆虫免疫系统用于保护自己的酵素。
虽然这种基因对基因的交互作用在疾病中是非常普遍的，但是病原菌中的单一基因瞄准动物或人类宿主的单一基因的例子，是非常罕见的。
只需极少量的发光杆菌就会杀死昆虫，大约10-100 个细菌就足够了，但是对于人类是无害的，因此可以利用发光杆菌当成取代杀虫剂的生物控制机制。
巴恩大学的研究人员Bristol and Exeter利用Manduca sexta这种昆虫研究细菌的剧毒基因。研究人员可以研究细菌的整个基因组，以了解它如何杀死宿主。
昆虫的免疫系统中使用一种名为对酚氧化酶(phenoloxidase)的酵素，可以杀死细菌并且将它们浓缩成致密的黑色素外套。研究员发现发光杆菌会制造一种特殊的对酚氧化酶抑制剂，以保护自己免受这种酵素的攻击。他们辨出抑制剂中的一个小分子1,3-dihydroxy-2-(isopropyl)-5-(2-phenylethenyl)benzene，缩写为ST，这个分子也是发光杆菌制造的抗生素，可用于杀死已死亡的昆虫尸体上的其它微生物一旦细菌没有了ST，毒性就减弱了。研究人员利用RNA干扰技术阻止昆虫制造对酚氧化酶，这些昆虫对于发光杆菌的敏感性更高。但是当昆虫无法制造对酚氧化酶，发光杆菌是否具有制造ST的能力，就变得没有影响。
（编译/姜欣慧） (资料来源 : biocompare)
英文原文链接：
http://news.biocompare.com/newsstory.asp?id=181333
原始出处：
Published online before print February 6, 2007, 10.1073/pnas.0610525104
PNAS | February 13, 2007 | vol. 104 | no. 7 | 2419-2424
An antibiotic produced by an insect-pathogenic bacterium suppresses host defenses through phenoloxidase inhibition
Ioannis Eleftherianos*, Sam Boundy*, Susan A. Joyce*, Shazia Aslam*, James W. Marshall, Russell J. Cox, Thomas J. Simpson, David J. Clarke*, Richard H. ffrench-Constant, and Stuart E. Reynolds*,
*Department of Biology and Biochemistry, University of Bath, Bath BA2 7AY, United Kingdom; School of Chemistry, University of Bristol, Bristol BS8 1TS, United Kingdom; and Centre for Ecology and Conservation, University of Exeter, Cornwall Campus, Penryn TR10 9EZ, United Kingdom
Communicated by David L. Denlinger, Ohio State University, Columbus, OH, December 7, 2006 (received for review April 25, 2006)
Photorhabdus is a virulent pathogen that kills its insect host by overcoming immune responses. The bacterium also secretes a range of antibiotics to suppress the growth of other invading microorganisms. Here we show that Photorhabdus produces a small-molecule antibiotic (E)-1,3-dihydroxy-2-(isopropyl)-5-(2-phenylethenyl)benzene (ST) that also acts as an inhibitor of phenoloxidase (PO) in the insect host Manduca sexta. The Photorhabdus gene stlA encodes an enzyme that produces cinnamic acid, a key precursor for production of ST, and a mutation in stlA results in loss of ST production and PO inhibitory activity, which are both restored by genetic complementation of the mutant and also by supplying cinnamic acid. ST is produced both in vitro and in vivo in sufficient quantities to account for PO inhibition and is the only detectable solvent-extractable inhibitor. A Photorhabdus stlA– mutant is significantly less virulent, proliferates slower within the host, and provokes the formation of significantly more melanotic nodules than wild-type bacteria. Virulence of the stlA– mutant is also rescued by supplying cinnamic acid. The proximate cause of the virulence effect, however, is the inhibition of PO, because the effect of the stlA– mutation on virulence is abolished in insects in which PO has been knocked down by RNA interference (RNAi). Thus, ST has a dual function both as a PO inhibitor to counter host immune reactions and also as an antibiotic to exclude microbial competitors from the insect cadaver.
Photorhabdus luminescens | RNA interference | stilbene | virulence
