## 1 Introduction  
Female flowers of cannabis (_Cannabis sativa_ L) possess a proliferous number of 'pellate' stalked glandular trichomes (GTs) on their surface [1, 2, 3]. These defensive structures develop predominantly in conjunction with female floral tissue and provide protection [4, 5, 6] by producing and storing large amounts of secondary metabolites, which include cannabinoids [1, 7]. These metabolites are particularly interesting due to their medicinal properties, acting via the human endocannabinoid and central nervous systems [8, 9]. Cannabis GTs have a basic morphology composed of a base that attaches to the floral epidermis, a multicellular stalk that extends outwards to act as conduit for photoassimilate transport and a globular head that is supported by the stalk [2, 10]. The GT head is composed of a ring of non-photosynthetic secretory disc cells that synthesise secondary metabolites that are then stored in an extracellular storage cavity that sits adaxially to the disc cells [11]. Attaching the disc to the stalk is a cluster of photosynthetic stipe cells that sit at the centre of the disc cell ring. The cannabinoid biosynthetic pathway is highly active in the disc cells [10] and is fed by the polyketide and methyleryth nitold 4-phosphate (MEP) pathways that provide olivetolic acid and geranyl pyrophosphate (GPP), respectively, for the synthesis of cannabinoid acid (CBGA), the first cannabinoid synthesised in the pathway [12]. The fatty acid hexanoic acid is the initial precursor of the cytosolically located polyketide pathway that is used to synthesise OA by way of hexanoyl-CoA synthetase, tetraketide synthase (TKS), and finally olivetolic acid cyclase (OAC) [13; 14]. CBGA is then synthesised in leucoplasts by aromatic prenyltransferases, one of which being aromatic prenyltransferase 1 (CsPT1) [12], and is then transported to the storage cavity where outer cell wall-bound [11] tetrahydroocannabinolic acid synthases (THCAS) synthesise THCA from CBGA [15]. CBGA is also a precursor for other cannabinoids [16; 17; 18] such as cannabidiolic acid (CBDA) and cannabichromeic acid (CBCA). 'Acid-form' cannabinoids can be converted into their 'neutral-form' by auto-decarboxylation [1]. In addition, cannabis is a genetically diverse species with a wide range of chemovars [19; 20], with differing GT sizes between highly cannabinoid productive modern cultivars and lower productive traditional landraces [5]. Regulation of arabidopsis (_Arabidopsis thaliana_) unicellular trichome development is well characterised, wherein the heterotrimeric MYB/bHLH/WD40 (MBW) complex acts as an activator/suppressor of GLABRA2 (GL2) to initiate trichome formation [21]. The MBW complex and GL2 act as central regulators for trichome development as they integrate together multiple phytohormonal signalling pathways, including jasmonic acid (JA), salicylic acid (SA), gibberell acid (GA), ethylene (ETH), and cytokins [22; 23]. In contrast, regulation of multicellular trichome development is not as well understood, but recent advances have shown that the same regulatory nodes are likely broadly conserved between distantly related species [24]. Amongst phytohormones of interest, JA is often a focus of study, having been shown to stimulate both glandular and non-glandular trichome initiation in artemisinin (_Artemisia annua_ L) [25], arabidopsis [26], and tomato (_Solanum Lyopersicum_ L) [27]. Moreover, JA was recently demonstrated to induce increased floral cannabinoid content [28] and trichome density [29] in cannabis. Other phytohormones have been studied for their effects on trichomes. One study found that application of either auxins, GA, or JA uniformly increased non-glandular trichome density on arabidopsis and poplar (_Populus trichocarpa_), but did not increase the amount of all trichome types on tomato [23]. In another study, brassinosteroids caused tomato glandular trichome density to decrease by inhibiting JA signalling [30].