# Unraveling the Complexity of Plant Trichomes: Models, Mechanisms, and Bioengineering Strategies
## 4 Glandular Secretory Trichomes (GSTs): Natural Biofactories
### Regulatory Mechanism of GSTs Development  
Although there are many plants containing GSTs, given the identification of complete genomes and plant genetic transformation systems, most research has focused on _Artemisia annua_ and multicellular tomato GSTs; in recent years, GST transcriptional regulatory networks have been further refined, and significant advances have been made in cellular information exchange and cell fate determination. _Cannabis_' regulatory network for GT development has not yet been explored. In recent studies, transcriptomics was analyzed in 8-week-old female flowers of _Cannabis sativa_ and revealed that GT development is a highly coordinated process regulated at the transcriptional level by the WRKY, MYB, bHLH, and ERF families. _CsMYC4_ was identified as a key gene that controls GT formation through MeJA signaling [37]. The molecular regulation of the glandular secretory trichomes of _Artemisia annua_ has been elucidated in recent studies. It has been determined that the HD-ZIP IV transcription factors AaHD1 and AaHD8, which have been identified in _Artemisia annua_, positively regulate GST production. In addition, AaHD8 promotes the expression of _AaHD1_ via jasmonic acid (JA) signaling [31; 43]. GST initiation is activated by the JA-responsive transcription factor AaSPL9 [44]. R2R3-MYB BaMYB17, which is expressed in shoot tip trichomes, is a GST-specific positive regulator [45]. In GST basal cells, AaMIXTA1 plays a critical role in promoting both GST initiation and artemisinin synthesis, while regulating the synthesis of leaf cuticles [46]. AaGSW2, a GST-specific factor, is directly activated by AaHD1/AaHD8; its overexpression increases GST density and artemisinin concentrations [47]. Through interaction with AaMIXTA1 and the indirect upregulation of AaGSW2, AaWIN1 increases GST density [48]. In contrast, AaMYB16 and AaMYB5 are negative regulators. AaGSW2 is not directly controlled by either of these genes, but both affect AaHD1's binding affinity to AaGSW2 [30]. MADS-box factor AaSEP1 promotes GST initiation by integrating JA and developmental signals. By interacting with AaMYB16, it amplifies the AaHD1-mediated activation of the AaGSW2 promoter, thereby increasing GST density and the production of artemisinin [49]. AaTA2, a R2R3-MYB factor, also promotes GST development and terpene/flavonoid synthesis. Its expression is directly enhanced by AaHD1 and AaHD8 [50]. AaMYB1 is a member of the S13 subfamily and induces GST formation by activating GL1 and GL2, which also affect gibberellin GA4 metabolism [51]. Conversely, the AaTLR1-AaWOX1-AaTLR2 complex suppresses GST development through GA3 regulation [52]. In addition, TRICHOME AND ARTEMISININ REGULATOR 1 (TAR1) binds to the promoters of CYP71 AV1 and ADS, coregulating the development of GST and artemisinin production [53]. Tomato type I, IV, VI, and VII trichomes are GSTs. Wo, the key gene for tomato GST formation, was initially identified by map-based cloning. Woolly mutants (LA3186) have dense trichome layers due to gain-of-function mutations [54]. Wo gene protein-protein interactions facilitate the transition of cells from the G2 to M phase, thereby promoting epidermal trichome formation [55]. Further studies have been conducted over the past decade to examine the roles of related transcription factors in regulating the differentiation of different types of trichomes in tomatoes. These transcription factors include those associated with the R2R3-MYB, HD-Zip IV, C2H2, and bHLH gene families [56; 57; 58]. Studies demonstrate that applying exogenous jasmonic acid (JA) to developing tomato leaves increases type VI glandular trichome density, enhancing secretory capacity and reducing thrips damage [59]. The JA signaling repressor SIJAZZ inhibits glandular trichome initiation by suppressing the expression of SIWo and SICycB2 [60]. GST development (types I + VI) in tomato is positively regulated by the F-box protein SICOI.