{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T19:24:23Z","timestamp":1790364263264,"version":"4.1.0"},"reference-count":77,"publisher":"American Society for Microbiology","issue":"9","license":[{"start":{"date-parts":[[2007,9,1]],"date-time":"2007-09-01T00:00:00Z","timestamp":1188604800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Eukaryot Cell"],"published-print":{"date-parts":[[2007,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Among eukaryotes, only slime molds, fungi, and plants contain signal transduction phosphorelay systems. In filamentous fungi, multiple sensor kinases appear to use a single histidine-containing phosphotransfer (HPt) protein to relay signals to two response regulators (RR). In\n            <jats:italic>Aspergillus nidulans<\/jats:italic>\n            , the RR SskA mediates activation of the mitogen-activated protein kinase SakA in response to osmotic and oxidative stress, whereas the functions of the RR SrrA were unknown. We used a genetic approach to characterize the\n            <jats:italic>srrA<\/jats:italic>\n            gene as a new member of the\n            <jats:italic>skn7\/prr1<\/jats:italic>\n            family and to analyze the roles of SrrA in the phosphorelay system composed of the RR SskA, the HPt protein YpdA, and the sensor kinase NikA. While mutants lacking the HPt protein YpdA are unviable, mutants lacking SskA (\u0394\n            <jats:italic>sskA<\/jats:italic>\n            ), SrrA (\u0394\n            <jats:italic>srrA<\/jats:italic>\n            ), or both RR (\u0394\n            <jats:italic>srrA<\/jats:italic>\n            \u0394\n            <jats:italic>sskA<\/jats:italic>\n            ) are viable and differentially affected in osmotic and oxidative stress responses. Both RR are involved in osmostress resistance, but \u0394\n            <jats:italic>sskA<\/jats:italic>\n            mutants are more sensitive to this stress, and only SrrA is required for H\n            <jats:sub>2<\/jats:sub>\n            O\n            <jats:sub>2<\/jats:sub>\n            resistance and H\n            <jats:sub>2<\/jats:sub>\n            O\n            <jats:sub>2<\/jats:sub>\n            -mediated induction of catalase CatB. In contrast, both RR are individually required for fungicide sensitivity and calcofluor resistance and for normal sporulation and conidiospore viability. The \u0394\n            <jats:italic>srrA<\/jats:italic>\n            and \u0394\n            <jats:italic>sskA<\/jats:italic>\n            sporulation defects appear to be related to decreased mRNA levels of the key sporulation gene\n            <jats:italic>brlA<\/jats:italic>\n            . In contrast, conidiospore viability defects do not correlate with the activity of the spore-specific catalase CatA. Our results support a model in which NikA acts upstream of SrrA and SskA to transmit fungicide signals and to regulate asexual sporulation and conidiospore viability. In contrast, NikA appears dispensable for osmotic and oxidative stress signaling. These results highlight important differences in stress signal transmission among fungi and define a phosphorelay system involved in oxidative and osmotic stress, cell wall maintenance, fungicide sensitivity, asexual reproduction, and spore viability.\n          <\/jats:p>","DOI":"10.1128\/ec.00085-07","type":"journal-article","created":{"date-parts":[[2007,7,14]],"date-time":"2007-07-14T01:10:41Z","timestamp":1184375441000},"page":"1570-1583","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":111,"title":["Response Regulators SrrA and SskA Are Central Components of a Phosphorelay System Involved in Stress Signal Transduction and Asexual Sporulation in\n            <i>Aspergillus nidulans<\/i>"],"prefix":"10.1128","volume":"6","author":[{"given":"Itzel","family":"Vargas-Pe\u0301rez","sequence":"first","affiliation":[{"name":"Departamento de Gene\u0301tica Molecular, Instituto de Fisiologi\u0301a Celular, Universidad Nacional Auto\u0301noma de Me\u0301xico, Apartado Postal 70-242, 04510, Me\u0301xico, D.F., Me\u0301xico"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Olivia","family":"Sa\u0301nchez","sequence":"additional","affiliation":[{"name":"Departamento de Gene\u0301tica Molecular, Instituto de Fisiologi\u0301a Celular, Universidad Nacional Auto\u0301noma de Me\u0301xico, Apartado Postal 70-242, 04510, Me\u0301xico, D.F., Me\u0301xico"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laura","family":"Kawasaki","sequence":"additional","affiliation":[{"name":"Departamento de Gene\u0301tica Molecular, Instituto de Fisiologi\u0301a Celular, Universidad Nacional Auto\u0301noma de Me\u0301xico, Apartado Postal 70-242, 04510, Me\u0301xico, D.F., Me\u0301xico"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dimitris","family":"Georgellis","sequence":"additional","affiliation":[{"name":"Departamento de Gene\u0301tica Molecular, Instituto de Fisiologi\u0301a Celular, Universidad Nacional Auto\u0301noma de Me\u0301xico, Apartado Postal 70-242, 04510, Me\u0301xico, D.F., Me\u0301xico"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jesu\u0301s","family":"Aguirre","sequence":"additional","affiliation":[{"name":"Departamento de Gene\u0301tica Molecular, Instituto de Fisiologi\u0301a Celular, Universidad Nacional Auto\u0301noma de Me\u0301xico, Apartado Postal 70-242, 04510, Me\u0301xico, D.F., Me\u0301xico"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(88)90198-5"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/MMBR.62.1.35-54.1998"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2958.1993.tb01565.x"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1080\/13693780600900080"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.tim.2005.01.007"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1574-6968.1999.tb13650.x"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.e06-02-0113"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cub.2005.08.061"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1128\/MMBR.68.1.1-108.2004"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/19.11.3105"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1994.tb06849.x"},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.1091\/mbc.12.2.407"},{"key":"e_1_3_2_14_2","doi-asserted-by":"publisher","DOI":"10.1093\/genetics\/143.1.155"},{"key":"e_1_3_2_15_2","doi-asserted-by":"publisher","DOI":"10.1128\/EC.2.6.1151-1161.2003"},{"key":"e_1_3_2_16_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrmicro1426"},{"key":"e_1_3_2_17_2","doi-asserted-by":"publisher","DOI":"10.1093\/genetics\/63.2.317"},{"key":"e_1_3_2_18_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2958.2005.04605.x"},{"key":"e_1_3_2_19_2","doi-asserted-by":"publisher","DOI":"10.1128\/AEM.68.11.5304-5310.2002"},{"key":"e_1_3_2_20_2","doi-asserted-by":"publisher","DOI":"10.1038\/nature04341"},{"key":"e_1_3_2_21_2","doi-asserted-by":"publisher","DOI":"10.1128\/JB.182.9.2428-2437.2000"},{"key":"e_1_3_2_22_2","doi-asserted-by":"publisher","DOI":"10.1271\/bbb.60665"},{"key":"e_1_3_2_23_2","doi-asserted-by":"publisher","DOI":"10.1271\/bbb.70051"},{"key":"e_1_3_2_24_2","unstructured":"Free radicals in biology and medicine 1989"},{"key":"e_1_3_2_25_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2958.2002.02774.x"},{"key":"e_1_3_2_26_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5193(05)80222-X"},{"key":"e_1_3_2_27_2","first-page":"20","volume":"48","year":"2001","unstructured":"Hill, T. 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