The Arabidopsis LEAFY COTYLEDON1 (LEC1) gene is required for the specification of cotyledon identity and the completion of embryo maturation. We isolated the LEC1 gene and showed that it functions at an early developmental stage to maintain embryonic cell fate. The LEC1 gene encodes a transcription factor homolog, the CCAAT box-binding factor HAP3 subunit. LEC1 RNA accumulates only during seed development in embryo cell types and in endosperm tissue. Ectopic postembryonic expression of the LEC1 gene in vegetative cells induces the expression of embryo-specific genes and initiates formation of embryo-like structures. Our results suggest that LEC1 is an important regulator of embryo development that activates the transcription of genes required for both embryo morphogenesis and cellular differentiation.

Arabidopsis LEAFY COTYLEDON1 (LEC1) is a critical regulator required for normal development during the early and late phases of embryogenesis that is sufficient to induce embryonic development in vegetative cells. LEC1 encodes a HAP3 subunit of the CCAAT binding transcription factor. We show that the 10 Arabidopsis HAP3 (AHAP3) subunits can be divided into two classes based on sequence identity in their central, conserved B domain. LEC1 and its most closely related subunit, LEC1-LIKE (L1L), constitute LEC1-type AHAP3 subunits, whereas the remaining AHAP3 subunits are designated non-LEC1-type. Similar to LEC1 , L1L is expressed primarily during seed development. However, suppression of L1L gene expression induced defects in embryo development that differed from those of lec1 mutants, suggesting that LEC1 and L1L play unique roles in embryogenesis. We show that L1L expressed under the control of DNA sequences flanking the LEC1 gene suppressed genetically the lec1 mutation, suggesting that the LEC1-type B domains of L1L and LEC1 are critical for their function in embryogenesis. Our results also suggest that LEC1-type HAP3 subunits arose from a common origin uniquely in plants. Thus, L1L, an essential regulator of embryo development, defines a unique class of plant HAP3 subunits.

LEAFY COTYLEDON1 (LEC1), an atypical subunit of the nuclear transcription factor Y (NF-Y) CCAAT-binding transcription factor, is a central regulator that controls many aspects of seed development including the maturation phase during which seeds accumulate storage macromolecules and embryos acquire the ability to withstand desiccation. To define the gene networks and developmental processes controlled by LEC1, genes regulated directly by and downstream of LEC1 were identified. We compared the mRNA profiles of wild-type and -null mutant seeds at several stages of development to define genes that are down-regulated or up-regulated by the mutation. We used ChIP and differential gene-expression analyses in seedlings overexpressing LEC1 and in developing and soybean seeds to identify globally the target genes that are transcriptionally regulated by LEC1 Collectively, our results show that LEC1 controls distinct gene sets at different developmental stages, including those that mediate the temporal transition between photosynthesis and chloroplast biogenesis early in seed development and seed maturation late in development. Analyses of enriched DNA sequence motifs that may act as-regulatory elements in the promoters of LEC1 target genes suggest that LEC1 may interact with other transcription factors to regulate distinct gene sets at different stages of seed development. Moreover, our results demonstrate strong conservation in the developmental processes and gene networks regulated by LEC1 in two dicotyledonous plants that diverged ∼92 Mya.

Background: Plant-specific IQD genes encode putative CaM targets of unknown functions. Results: IQD1 interacts with KLCR1, binds to Arabidopsis CaM/CMLs, and localizes to microtubules. Conclusion: IQD1 may act as a scaffold protein recruiting cargo to kinesin motors for directional transport along microtubules. Significance: This work provides novel insight into IQD function and a framework to study plant kinesin regulation.

Ionic regulation and acid-base balance are fundamental to the physiology of vertebrates including fish. Acidification of freshwater ecosystems is recognized as a global environmental problem, and the physiological responses to acid exposure in a few fish species are well characterized. However, the underlying mechanisms promoting ionic and acid-base balance for most fish species that have been investigated remain unclear. Zebrafish (Danio rerio) has emerged as a powerful model system to elucidate the molecular basis of ionic and acid-base regulation. The utility of zebrafish is related to the ease with which it can be genetically manipulated, its suitability for state-of-the-art molecular and cellular approaches, and its tolerance to diverse environmental conditions. Recent studies have identified several key regulatory mechanisms enabling acclimation of zebrafish to acidic environments, including activation of the sodium/hydrogen exchanger (NHE) and H + -ATPase for acid secretion and Na + uptake, cortisol-mediated regulation of transcellular and paracellular Na + movements, and ionocyte proliferation controlled by specific cell-fate transcription factors. These integrated physiological responses ultimately contribute to ionic and acid-base homeostasis in zebrafish exposed to acidic water. In the present review, we provide an overview of the general effects of acid exposure on freshwater fish, the adaptive mechanisms promoting extreme acid tolerance in fishes native to acidic environments, and the mechanisms regulating ionic and acid-base balance during acid exposure in zebrafish. KEY WORDS: Acid exposure, Acid-base balance, Ionic regulation, Zebrafish IntroductionDeclining fish populations in acidified lakes and streams (see review by McDonald, 1983a) was a significant factor promoting intensive research over the past 40 years on the ecological and physiological consequences of aquatic acidification. In freshwater (FW) ecosystems, acidification is caused largely by atmospheric acidic deposition (i.e. acid rain). Acidification of FW is a global problem, which has been documented in several geographic regions including eastern Europe, the USA and China (Psenner, 1994;Schindler, 1988;Wright et al., 2005). In Canada, it is estimated that about 40% of lakes are in regions susceptible to acid deposition (Kelso et al., 1990). Most aquatic animals, including fish, live in a narrow range of pH near neutrality, and acute or chronic exposure to acidic water can adversely affect their physiological functions (McDonald, 1983a;Wood, 1989). Nevertheless, some species thrive in acidic environments, and thus can serve as useful models for investigating the mechanisms underlying adaptation to acid stress. REVIEWDepartment of Biology, University of Ottawa, 30 Marie Curie, Ottawa, ON, Canada, K1N 6N5.*Author for correspondence (wkwong@uottawa.ca)The mechanisms of ionic and acid-base regulation in fish have been summarized in previous reviews (Claiborne et al., 2002;Evans et al., 2005;Gilmour and Perry, 2009;Goss et al., 19...