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			<titleStmt><title level='a'>Characterizing host-pathogen interactions between Zostera marina and Labyrinthula zosterae</title></titleStmt>
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				<publisher>Frontiers of Marine Science</publisher>
				<date>08/08/2023</date>
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				<bibl> 
					<idno type="par_id">10531841</idno>
					<idno type="doi">10.3389/fmars.2023.1152647</idno>
					<title level='j'>Frontiers in Marine Science</title>
<idno>2296-7745</idno>
<biblScope unit="volume">10</biblScope>
<biblScope unit="issue"></biblScope>					

					<author>Yaamini R Venkataraman</author><author>Amanda Shore</author><author>Sukanya Dayal</author><author>James Sanghyun Lee</author><author>Mahsa Alidoost_Salimi</author><author>Grace Crandall</author><author>Malina M Loeher</author><author>Mark Stoops</author><author>Megan Swanger</author><author>Morgan E Eisenlord</author><author>Kathryn L Van_Alstyne</author><author>Mark D Fast</author><author>Colleen A Burge</author><author>Maya L Groner</author>
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			<abstract><ab><![CDATA[<sec><title>Introduction</title><p>Seagrass meadows serve as an integral component of coastal ecosystems but are declining rapidly due to numerous anthropogenic stressors including climate change. Eelgrass wasting disease, caused by opportunistic<italic>Labyrinthula</italic>spp., is an increasing concern with rising seawater temperature. To better understand the host-pathogen interaction, we paired whole organism physiological assays with dual transcriptomic analysis of the infected host and parasite.</p></sec> <sec><title>Methods</title><p>Eelgrass (<italic>Zostera marina</italic>) shoots were placed in one of two temperature treatments, 11° C or 18° C, acclimated for 10 days, and exposed to a waterborne inoculation containing infectious<italic>Labyrinthula zosterae</italic>(<italic>Lz</italic>) or sterile seawater. At two- and five-days post-exposure, pathogen load, visible disease signs, whole leaf phenolic content, and both host- and pathogen- transcriptomes were characterized.</p></sec> <sec><title>Results</title><p>Two days after exposure, more than 90% of plants had visible lesions and<italic>Lz</italic>DNA was detectable in 100% percent of sampled plants in the<italic>Lz</italic>exposed treatment. Concentrations of total phenolic compounds were lower after 5 days of combined exposure to warmer temperatures and<italic>Lz</italic>, but were unaffected in other treatments. Concentrations of condensed tannins were not affected by<italic>Lz</italic>or temperature, and did not change over time. Analysis of the eelgrass transcriptome revealed 540 differentially expressed genes in response to<italic>Lz</italic>exposure, but not temperature.<italic>Lz</italic>-exposed plants had gene expression patterns consistent with increased defense responses through altered regulation of phytohormone biosynthesis, stress response, and immune function pathways. Analysis of the pathogen transcriptome revealed up-regulation of genes potentially involved in breakdown of host defense, chemotaxis, phagocytosis, and metabolism.</p></sec> <sec><title>Discussion</title><p>The lack of a significant temperature signal was unexpected but suggests a more pronounced physiological response to<italic>Lz</italic>infection as compared to temperature. Pre-acclimation of eelgrass plants to the temperature treatments may have contributed to the limited physiological responses to temperature. Collectively, these data characterize a widespread physiological response to pathogen attack and demonstrate the value of paired transcriptomics to understand infections in a host-pathogen system.</p></sec>]]></ab></abstract>
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<div xmlns="http://www.tei-c.org/ns/1.0"><head>O n e s p e cifi c p at h w a y i n w hi c h A B A aff e cts pl a nt d ef e ns e is i n t h e c all os e p at h w a y, w hi c h is i n v ol v e d i n d ef e ns e of f u n g al p at h o g e ns i n pl a nts. S p e cifi c all y, A B A m ut a nts dis pl a y e d i m p air e d r esist a n c e t o n e cr otr o p hi c f u n gi, a n d A B A a d diti o n t o t h e i nf e cti o n sit e mi mi c k e d c all os e d e p ositi o n a n d i n cr e as e d r esist a n c e t o n e cr otr o p hi c f u n gi (M a u c h-M a ni a n d M a u c h, 2 0 0 5 ). T h er ef or e, it is n ot s ur prisi n g t o o bs er v e alt er e d A B A e x pr essi o n i n Z. m ari n a i nf e ct e d wit h L z , w hi c h h as n e cr oti c c a p a biliti es.</head><p>A   <ref type="table">( 2 1 0 9 6 0 7;</ref> <ref type="table">1 2 1 5 9 7 7</ref>  <ref type="table">5 3</ref>, <ref type="table">4 0 1 -4 0 9. d oi:  1 0. 1 0 1 6/ 0 0 2 2-2 0 1 1( 8 9) 9 0 1 0 6</ref>  <ref type="table">3 4</ref>, <ref type="table">6 7 -7 5. d oi: 1 0. 1 0 4 6/  j. 1 3 6 5-3 1 3 X. 2 0 0 3. 0 1 7 0 7</ref>  <ref type="table">1</ref><ref type="table">2</ref>  <ref type="table">5 7</ref>, <ref type="table">1 1 8 7 -1 1 9 5. d oi: 1 0. 1 0 1 6/ S 0 0 3 1-9 4 2 2( 0 1)  0 0 0 5 3</ref> Bi ol. Cell 1 7, 3 9 2 1 -3 9 2 9. d oi: 1 0. 1 0 9 1/ m b c. e 0 6-0 5-0 3 8 1 V er g e er, L. H. T., A arts, T. L., a n d D e Gr o ot, J. D. ( 1 9 9 5). T h e 'w asti n g dis e as e 'a n d t h e eff e ct of a bi oti c f a ct ors (li g ht i nt e nsit y, t e m p er at ur e, s ali nit y) a n d i nf e cti o n wit h L a b yri nt h ul a z oster ae o n t h e p h e n oli c c o nt e nt of Z oster a m ari n a s h o ots. A q u at. B ot. 5 2, 3 5 -4 4. d oi: 1 0. 1 0 1 6/ 0 3 0 4-3 7 7 0( 9 5) 0 0 4 8 0-N V er g e er, L. H., a n d D e v eli, A. ( 1 9 9 7). P h e n oli c a ci ds i n h e alt h y a n d i nf e ct e d l e a v es of Z oster a m ari n a a n d t h eir gr o wt h-li miti n g pr o p erti es t o w ar ds L a b yri nt h ul a z oster ae . A q u at. B ot. 5 8, 6 5 -7 2. d oi: 1 0. <ref type="table">1</ref><ref type="table">2</ref><ref type="table">3</ref> </p></div>
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