In plants, as in animals, programmed cell death (PCD) is a key process responsible for the elimination of unneeded structures and for overall shape remodeling during development [1]; however, the molecular mechanisms remain poorly understood. Despite the absence of canonical caspases in plants, dying plant cells show an increased proteolytic caspase-like activity [2]. Moreover, the cell death can be suppressed using synthetic [2] or natural [3] caspase inhibitors. This raises the question of whether plants have specific cysteine proteases with a role similar to metazoan caspases in the execution of PCD. Metacaspases are the best candidates to perform this role, because they contain a caspasespecific catalytic diad of histidine and cysteine as well as conserved caspase-like secondary structure [4,5]. Here we show the first experimental evidence for metacaspase function in the activation and/or execution of PCD in plants, and also demonstrate the fundamental requirement of plant metacaspase for embryogenesis.We explored the role of plant metacaspases in PCD using a model system of somatic embryogenesis of Norway spruce (Picea abies), where the pathway of embryo development (Figure 1A) resembles zygotic embryogeny, even though the embryo origin is different in each case (i.e., somatic cells in proembryogenic mass

Growth in perennial plants possesses an annual cycle of active growth and dormancy that is controlled by environmental factors, mainly photoperiod and temperature. In conifers and other nonangiosperm species, the molecular mechanisms behind these responses are currently unknown. In Norway spruce (Picea abies L. Karst.) seedlings, growth cessation and bud set are induced by short days and plants from southern latitudes require at least 7 to 10 h of darkness, whereas plants from northern latitudes need only 2 to 3 h of darkness. Bud burst, on the other hand, is almost exclusively controlled by temperature. To test the possible role of Norway spruce FLOWERING LOCUS T (FT)-like genes in growth rhythm, we have studied expression patterns of four Norway spruce FT family genes in two populations with a divergent bud set response under various photoperiodic conditions. Our data show a significant and tight correlation between growth rhythm (both bud set and bud burst), and expression pattern of one of the four Norway spruce phosphatidylethanolamine-binding protein gene family members (PaFT4) over a variety of experimental conditions. This study strongly suggests that one Norway spruce homolog to the FT gene, which controls flowering in angiosperms, is also a key integrator of photoperiodic and thermal signals in the control of growth rhythms in gymnosperms. The data also indicate that the divergent adaptive bud set responses of northern and southern Norway spruce populations, both to photoperiod and light quality, are mediated through PaFT4. These results provide a major advance in our understanding of the molecular control of a major adaptive trait in conifers and a tool for further molecular studies of adaptive variation in plants.Trees and other perennial plants must adapt their growth rhythm to seasonal changes in the environment. To a large extent, this adaptation is genetically controlled (Howe et al., 2003). A clear example is the strong clinal pattern of growth cessation and bud set in seedlings of the conifer Norway spruce (Picea abies L. Karst.; Ekberg et al., 1976).Like most conifers, Norway spruce has a long juvenile phase of about 20 years before the first cones are formed. In first-year seedlings, the annual cycle (Fig. 1) can be summarized as (1) shoot extension stops and terminal buds are set in late summer in response to a shortening photoperiod, after which the cambium ceases growth, needle primordia are initiated within the buds, and frost tolerance begins to increase; (2) rest dormancy (endodormancy) develops in the meristems during autumn after bud set and, with exposure to chilling temperatures (2°C-10°C), changes into quiescence dormancy (ectodormancy) by midwinter, when frost tolerance is maximal; and (3) opening of the bud scales (bud burst) occurs in spring after a temperature sum (TS) has been attained. The extension growth of first-year seedlings consists of the expansion of stem units formed in the current season. This free growth is in the following years (Fig.

Metacaspase-dependent autophagy in plants promotes cell disassembly during vacuolar cell death and inhibits necrosis.

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