<?xml version="1.0" encoding="ISO-8859-1"?><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
<front>
<journal-meta>
<journal-id>1405-888X</journal-id>
<journal-title><![CDATA[TIP. Revista especializada en ciencias químico-biológicas]]></journal-title>
<abbrev-journal-title><![CDATA[TIP]]></abbrev-journal-title>
<issn>1405-888X</issn>
<publisher>
<publisher-name><![CDATA[Universidad Nacional Autónoma de México, Facultad de Estudios Superiores Zaragoza]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S1405-888X2024000100012</article-id>
<article-id pub-id-type="doi">10.22201/fesz.23958723e.2024.659</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[PHR1 como componente central en el balance entre la respuesta a la deficiencia de fosfato y la respuesta inmune en plantas]]></article-title>
<article-title xml:lang="en"><![CDATA[PHR1 as a central component in the balance between the response to phosphate deficiency and the immune response in plants]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[González-Coronel]]></surname>
<given-names><![CDATA[José Manuel]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Coello]]></surname>
<given-names><![CDATA[Patricia]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad Nacional Autónoma de México Facultad de Química Departamento de Bioquímica]]></institution>
<addr-line><![CDATA[Ciudad de México ]]></addr-line>
<country>Mexico</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>00</month>
<year>2024</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>00</month>
<year>2024</year>
</pub-date>
<volume>27</volume>
<fpage>0</fpage>
<lpage>0</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S1405-888X2024000100012&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S1405-888X2024000100012&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S1405-888X2024000100012&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen El fosfato (Pi) es esencial para el crecimiento de las plantas, pero su absorción es ineficiente debido a su limitada movilidad en el suelo y su conversión en formas insolubles. En respuesta a esta deficiencia, las plantas han desarrollado respuestas adaptativas conocidas como Respuestas a la Escasez de Fosfato (PSR), que implican adaptaciones fisiológicas y genéticas. La regulación genética de la PSR es fundamental, y el factor transcripcional PHR1 (Phosphate Starvation Response1) actúa como un modulador maestro que coordina múltiples vías de señalización. El control de la actividad de PHR1 ocurre a nivel post-traduccional mediante proteínas modificadoras de la subfamilia SPX. Adicionalmente, PHR1 es fosforilado en el residuo de S11 por cinasas de la familia SnRK1 y esta fosforilación tiene un efecto negativo en su actividad transcripcional. Se ha demostrado que PHR1 regula negativamente la expresión de diversos genes relacionados con la respuesta inmune, incluyendo a los que están involucrados en las vías del ácido jasmónico (JA) y del ácido salicílico (SA), que son cruciales en la defensa contra microorganismos que colonizan las raíces. Los estudios en comunidades microbianas sintéticas (SynCom) respaldan la idea de que las plantas establecen una respuesta funcional a la escasez del Pi gracias a la presencia de estos microorganismos. Para llevar a cabo esta función debe de existir un equilibrio entre la red de respuesta a la falta de nutrientes y la respuesta inmune que permite que estos organismos favorezcan la captación de nutrientes. Esta revisión destaca las características más importantes de PHR1, su papel en la estimulación de la respuesta a la falta del Pi y su capacidad de regular la expresión de genes implicados en la respuesta inmune. Los datos proporcionados ayudan a comprender que PHR1 representa un punto de convergencia que coordina e integra mecanismos de señalización para contender contra la falta del Pi, pero además regula la asociación con microorganismos que podrían ayudar en la captación del nutriente.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract Phosphate (Pi) is essential for plant growth, but its uptake is inefficient due to its limited mobility in the soil and its conversion into insoluble forms. In response to this deficiency, plants have developed adaptive responses known as Phosphate Starvation Responses (PSR) that involve physiological and genetic adaptations. Genetic regulation of PSR is critical, and the transcriptional factor PHR1 (Phosphate Starvation Response1) acts as a master modulator that coordinates multiple signaling pathways. Control of PHR1 activity occurs at the post-translational level by SPX modifying proteins. Additionally, PHR1 is phosphorylated at the S11 residue by kinases of the SnRK1 family and this phosphorylation has a negative effect on its transcriptional activity. PHR1 has been shown to directly downregulate the expression of genes related to the immune response, including several genes involved in the jasmonic acid (JA) and salicylic acid (SA) pathways, which are crucial in defense against root-colonizing microorganisms. Studies with synthetic microbial communities (SynCom) support the idea that plants establish a functional response to Pi deficiency due to the presence of microorganisms in their roots. To carry out this function, there must be a balance between the nutrient deficiency response network and the immune response that allows these organisms to favor the uptake of nutrients. This suggests that plant roots have evolved alongside beneficial microorganisms to deal with the lack of this nutrient. This review highlights the key features of PHR1, its role in stimulating the response to Pi deficiency, and its ability to regulate the expression of genes involved in the immune response. The provided data help to understand that PHR1 serves as a point of convergence, coordinating and integrating signaling mechanisms to combat the lack of Pi. Additionally, it regulates the association with microorganisms that could aid in the uptake of this nutrient.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Respuesta a la Escasez de Pi]]></kwd>
<kwd lng="es"><![CDATA[PHR1]]></kwd>
<kwd lng="es"><![CDATA[regulación post-traduccional]]></kwd>
<kwd lng="es"><![CDATA[respuesta inmune]]></kwd>
<kwd lng="en"><![CDATA[Phosphate Starvation Response]]></kwd>
<kwd lng="en"><![CDATA[PHR1]]></kwd>
<kwd lng="en"><![CDATA[post-translational regulation]]></kwd>
<kwd lng="en"><![CDATA[immune response]]></kwd>
</kwd-group>
</article-meta>
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