The genetic control of patterning in pea leaves

Expression patterns of class I KNOX and YABBY genes in Ruscus aculeatus (Asparagaceae) with implications for phylloclade homology

“…Furthermore, developmental genetic studies clarify that amalgamation of different developmental pathways obscures the boundary between the three major vegetative organs (root, stem, leaf) (Hofer, 1998;Sinha, 1999). These findings have led to recent re-evaluation of the importance of the Fuzzy Arberian Morphology (FAM) approach named after Agnes Arber (Rutishauser and Isler, 2001), such as the Leaf -Shoot Continuum Hypothesis (Arber, 1950).…”

Pea Compound Leaf Architecture Is Regulated by Interactions among the Genes UNIFOLIATA, COCHLEATA, AFILA, and TENDRIL-LESS

“…Previous authors have suggested that the AF gene either directs (Gould et al, 1994) or promotes (Lu et al, 1996;DeMason, 1997, 1999a;Hofer and Ellis, 1998) lamina formation in a wild-type pea leaf. Clearly, AF is not required for leaflet formation per se, because leaflets form on af tl, af uni (Marx, 1987), and af tl uni plants (Hofer and Ellis, 1996).…”

“…It was described previously that uni af and uni af tl leaves can be pentafoliate and thus more complex than uni leaves, which are trifoliate at their maximum complexity (Hofer and Ellis, 1998). An example of a uni af tl triple mutant leaf with a rachis and two pairs of leaflets is shown in Figure 7A.…”

Palmate-like pentafoliata1 encodes a novel Cys(2)His(2) zinc finger transcription factor essential for compound leaf morphogenesis in Medicago truncatula

“…The observation that PALM1 homologous sequences exist in lower land plants (our The expression was greatly reduced in older leaf primordia, consistent with their role in promoting a transient phase of indeterminacy required for leaflet initiation in these species. Although both UNI and SGL1 play a similar role in compound leaf development in pea and M. truncatula, leaflet primordia develop acropetally in pea with pinnate compound leaves and tendrils 19 but basipetally in M. truncatula with ternate leaves. 16 This suggests that differences in compound leaf development in closely related species may explain some differences in compound leaf phenotypes of loss-of-function uni mutants in pea and sgl1 mutants in M. truncatula.…”

“…15 In garden pea (Pisum sativum) and Medicago truncatula, both belonging to the inverted repeat lacking clade (IRLC) of legume, the role of KNOXI proteins in compound leaf development is replaced by the FLORICAULA (FLO)/ LEAFY (LFY) orthologs UNIFOLIATA (UNI) and SINGLE LEAFLET1 (SGL1), respectively. [16][17][18][19][20] This is mainly because (1) KNOXI proteins are not reactivated in compound leaf primordia in these plants and (2) loss-of-function mutants of UNI and SGL1 develop simplified or simple leaves. Interestingly, leaf developmental programs remain responsive to ectopically expressed KNOXI proteins in these species.…”