粗糙脉孢菌中组氨酸激酶响应香芹酚胁迫的作用机制  

Mechanism of histidine kinases in responses to carvacrol stress in Neurospora crassa

作　　者：陈鹏旭 蓝子依 席娟 陈莹莹 郑维发 赵艳霞 CHEN Pengxu;LAN Ziyi;XI Juan;CHEN Yingying;ZHENG Weifa;ZHAO Yanxia(School of Life Sciences,Jiangsu Normal University,Xuzhou 221116,Jiangsu,China)

机构地区：[1]江苏师范大学生命科学学院,江苏徐州221116

出　　处：《菌物学报》2025年第4期98-107,共10页Mycosystema

基　　金：国家自然科学基金(31971564);江苏师范大学2024年研究生科研与实践创新计划项目(2024XKT1512)。

摘　　要：以粗糙脉孢菌为研究材料,探究组氨酸激酶在应对香芹酚胁迫下的作用。通过比较不同组氨酸激酶(HKs)缺失菌株与野生型粗糙脉孢菌在受香芹酚胁迫后的形态变化、抑菌圈形成、超氧化物歧化酶(T-SOD)和过氧化氢酶(CAT)活性,以及类胡萝素的含量等,研究HKs在应对香芹酚胁迫中的作用。研究发现,除Δdcc1外,其他hk缺失菌株在香芹酚胁迫下均形成抑菌圈,且丙二醛(MDA)的形成量增加。检测具抗氧化能力的T-SOD和CAT活性发现,hcp1和sln1的敲除抑制了T-SOD的活性,os1、phy2和hk1的敲除抑制了CAT的活性,且香芹酚胁迫仅能激发野生型、Δhcp1、Δsln1、Δdcc1和Δhk16菌株中的T-SOD的活性,不能诱导Δhcp1、Δnik2、Δphy2、Δluxq、Δdcc1和Δhk16菌株中CAT的活性。类胡萝卜素是粗糙脉孢菌的主要组成成分且具抗氧化活性,hk9、os1、sln1、phy1、phy2、luxq、hk1和dcc1的缺失抑制了类胡萝卜素的合成,但是香芹酚的添加诱导Δsln1、Δluxq和Δhk16突变体中类胡萝卜素的合成。粗糙脉孢菌通过HKs感知环境中香芹酚的信号,通过调节T-SOD和CAT的活性以及类胡萝卜素的合成应对香芹酚的胁迫。The role of histidine kinases(HKs)in response to carvacrol stimulation in Neurospora crassa was investigated by comparing the morphological changes,the formation of growth-inhibition zone,total superoxide dismutase(T-SOD)and catalase(CAT)activities,as well as carotenoid content between different hk-deficient mutants and the wild-type N.crassa under carvacrol stress.hk-deficient strains,with the exception ofΔdcc1,exhibited a zone of growth-inhibition and increased malondialdehyde(MDA)synthesis under carvacrol stress.Analysis of T-SOD and CAT activities revealed that the deletion of hcp1 and sln1 resulted in inhibition of T-SOD activity,while the deletion of os1,phy2,and hk1 led to reduction of CAT activity.Carvacrol stress stimulated T-SOD activity in the wild-type strain andΔhcp1,Δsln1,Δdcc1,andΔhk16 mutants.However,it did not induce CAT activity in the strainsΔhcp1,Δnik2,Δphy2,Δluxq,Δdcc1,andΔhk16.Carotenoids are the main components within N.crassa and have antioxidant properties.It was observed that the deletion of hk9,os1,sln1,phy1,phy2,luxq,hk1,and dcc1 resulted in inhibition of carotenoid synthesis,but the carvacrol stress promoted the synthesis of carotenoids inΔsln1,Δluxq,andΔhk16 mutants.In summary,N.crassa responded to carvacrol stress by regulating the activities of T-SOD and CAT and the synthesis of carotenoids through HKs which sense the signal from carvacrol.

关 键 词：组氨酸激酶 香芹酚 类胡萝卜素 丙二醛 超氧化物歧化酶 

分 类 号：Q935[生物学—微生物学]