The Arabidopsis genome encodes for 10 Homeodomain-Leucine Zipper II (HD-Zip II) transcription factors that can be grouped into four clades (?-?). ATHB2, HAT1, HAT2 (g subfamily), HAT3 and ATHB4 (d subfamily) are all regulated by light quality changes that induce the shade avoidance response in most of the angiosperms (Ciarbelli et al., 2008). Intriguingly, it has recently emerged that besides their role in shade avoidance HD-Zip IIg and HD-Zip IId proteins play a crucial role in plant development from embryogenesis onwards in a white light environment. It has been indeed found that cotyledon development and number are altered in hat3 athb4 loss-offunction mutant embryos, and that these defects correlate with changes in auxin distribution and response, indicating a link between auxin-mediated embryo patterning and HD-Zip II function (Turchi et al., 2013; this work). Interestingly, it has also been shown that ATHB2 is induced in the HAT3-ATHB4 expression domain in the apical part of the embryo, marking the incipient cotyledons, as well as in the shoot apical meristem (SAM) of hat3 athb4, and thus can at least partially compensate for HAT3 and ATHB4 function. Consistent with ATHB2 being, to some extent, functionally interchangeable with HD-Zip II? proteins, it was observed that athb2 loss-offunction mutations enhance the hat3 athb4 phenotype. Indeed, hat3 athb4 athb2 mutants display one or two radialized cotyledons and lack an active SAM, resembling phenotypes associated with loss-of-function mutations in the HD-Zip III genes PHB, PHV and REV, master regulators of apical embryo development and primary determinants of adaxial cell fate (Turchi et al. 2013 and references therein). It has been then demonstrated that simultaneous lack of both HAT3 and ATHB4 is associated with loss of adaxial identity of lateral organs whereas ectopic expression of HAT3, ATHB4 or ATHB2 results in upward leaf curling, a phenotype similar to that seen when HD-Zip III genes are expressed in both adaxial and abaxial regions of lateral organs (Bou-Torrent et al., 2012; Turchi et al., 2013 and references therein; this work). The functional interaction between HD-Zip II and HD-Zip III genes has been further corroborated by the discovery that ATHB2 is directly positively regulated by REV in vivo (Turchi et al., 2013). Together, these findings demonstrate that members of the HD-Zip II protein family, mostly known for their role in shade avoidance, control embryo apical patterning, SAM activity and organ polarity interacting with HDZip III proteins.
HOMEODOMAIN-LEUCINE ZIPPER II FAMILY OF TRANSCRIPTION FACTORS CONTROL APICAL EMBRYO DEVELOPMENT, MERISTEM FUNCTION AND ORGAN POLARITY
TURCHI L;CARABELLI M;SASSI M;SESSA G;RUBERTI I
2013
Abstract
The Arabidopsis genome encodes for 10 Homeodomain-Leucine Zipper II (HD-Zip II) transcription factors that can be grouped into four clades (?-?). ATHB2, HAT1, HAT2 (g subfamily), HAT3 and ATHB4 (d subfamily) are all regulated by light quality changes that induce the shade avoidance response in most of the angiosperms (Ciarbelli et al., 2008). Intriguingly, it has recently emerged that besides their role in shade avoidance HD-Zip IIg and HD-Zip IId proteins play a crucial role in plant development from embryogenesis onwards in a white light environment. It has been indeed found that cotyledon development and number are altered in hat3 athb4 loss-offunction mutant embryos, and that these defects correlate with changes in auxin distribution and response, indicating a link between auxin-mediated embryo patterning and HD-Zip II function (Turchi et al., 2013; this work). Interestingly, it has also been shown that ATHB2 is induced in the HAT3-ATHB4 expression domain in the apical part of the embryo, marking the incipient cotyledons, as well as in the shoot apical meristem (SAM) of hat3 athb4, and thus can at least partially compensate for HAT3 and ATHB4 function. Consistent with ATHB2 being, to some extent, functionally interchangeable with HD-Zip II? proteins, it was observed that athb2 loss-offunction mutations enhance the hat3 athb4 phenotype. Indeed, hat3 athb4 athb2 mutants display one or two radialized cotyledons and lack an active SAM, resembling phenotypes associated with loss-of-function mutations in the HD-Zip III genes PHB, PHV and REV, master regulators of apical embryo development and primary determinants of adaxial cell fate (Turchi et al. 2013 and references therein). It has been then demonstrated that simultaneous lack of both HAT3 and ATHB4 is associated with loss of adaxial identity of lateral organs whereas ectopic expression of HAT3, ATHB4 or ATHB2 results in upward leaf curling, a phenotype similar to that seen when HD-Zip III genes are expressed in both adaxial and abaxial regions of lateral organs (Bou-Torrent et al., 2012; Turchi et al., 2013 and references therein; this work). The functional interaction between HD-Zip II and HD-Zip III genes has been further corroborated by the discovery that ATHB2 is directly positively regulated by REV in vivo (Turchi et al., 2013). Together, these findings demonstrate that members of the HD-Zip II protein family, mostly known for their role in shade avoidance, control embryo apical patterning, SAM activity and organ polarity interacting with HDZip III proteins.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
