Cytokinin-repressed ABA signaling

Plant Physiology Preview. Published on January 17, 2014, as DOI:10.1104/pp.113.234740

Running Head: Cytokinin-repressed ABA signaling

Corresponding authors:

Jianru Zuo

Institute of Genetics and Developmental Biology, Chinese Academy of Sciences

Datun Road, Beijing 100101, China

Tel: (+8610)6480 6585

Fax: (+8610)6480 6595

E-mail: jrzuo@https://www.wendangku.net/doc/bc12576859.html,

Research Area: Signaling and Response

Cytokinin antagonizes abscisic acid-mediated inhibition of cotyledon greening by promoting the degradation of ABI5 protein in Arabidopsis1

Chunmei Guan, Xingchun Wang, Jian Feng, Sulei Hong, Yan Liang, Bo Ren, Jianru Zuo*

State Key Laboratory of Plant Genomics and National Plant Gene Research Center, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China (C.G., J.F., S.H., Y.L., B.R. and J.Z.); University of Chinese Academy of Sciences, Beijing 100049, China (C.G., J.F. and S.H.); College of Life Sciences, Shanxi Agricultural University, Taigu, Shanxi 030801, China (X.W.).

One sentence summary:

Cytokinin represses ABA signaling by promoting ABI5 degradation in Arabidopsis.

Total word count: 9,003

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Footnotes

1 This work was supported by grants from the National Natural Science Foundation of China (90817107, 9121730

2 and 31100211) and the Ministry of Science of Technology of China (2014CB943400).

*Corresponding author e-mail: jrzuo@https://www.wendangku.net/doc/bc12576859.html,.

The author responsible for the distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (https://www.wendangku.net/doc/bc12576859.html,) is: Jianru Zuo (jrzuo@https://www.wendangku.net/doc/bc12576859.html,).

ABSTRACT

In higher plants, seed germination is followed by postgerminative growth. One of the key developmental events during postgerminative growth is cotyledon greening that enables a seedling establish the photosynthetic capacity. The plant phytohormone abscisic acid (ABA) plays a vital role by inhibiting seed germination and postgerminative growth in response to the dynamically changing internal and environmental cues. It has been shown that ABSCISIC ACID INSENSITIVE 5 (ABI5), a bZIP transcription factor, is an important factor in the regulation of ABA-mediated inhibitory effect on seed germination and postgerminative growth. Conversely, the phytohormone cytokinin has been proposed to promote seed germination by antagonizing ABA-mediated inhibitory effect. However, the underpinning molecular mechanism of the cytokinin-repressed ABA signaling is largely unknown. Here, we show that cytokinin specifically antagonizes ABA-mediated inhibition on cotyledon greening with minimal effects on seed germination in Arabidopsis (Arabidopsis thaliana). We found that the cytokinin-antagonized ABA effect is dependent on a functional cytokinin signaling pathway, mainly involved in the cytokinin receptor gene CRE1/AHK4, downstream AHP2, 3, 5 genes, and a type-B response regulator gene ARR12, which genetically acts upstream of ABI5 to regulate cotyledon greening. Cytokinin has no apparent effect on the transcription of ABI5. However, cytokinin efficiently promotes the proteasomal degradation of ABI5 protein in a cytokinin signaling-dependent manner. These results define a genetic pathway, through which cytokinin specifically induces the degradation of ABI5 protein, thereby antagonizing ABA-mediated inhibition on postgerminative growth.

Key words: ABA; ABI5; Arabidopsis; cotyledon greening; cytokinin signaling

INTRODUCTION

Seed germination and subsequent seedling establishment are key developmental events during plant growth. In Arabidopsis (Arabidopsis thaliana), seed germination is morphologically characterized by several distinctive phases, including testa rupture, endosperm rupture and radicle protrusion (Bewley, 1997; Müller et al., 2006; Piskurewicz et al., 2008). During seed germination, a major physiological event is the degradation and mobilization of the storage compounds that are accumulated during seed maturation and are used for the energy supply of a seed during germination. These processes are under the tight control of the genetic programs and are regulated by the environmental factors, including light, temperature and osmotic stress (Bewley, 1997; Lopez-Molina et al., 2001; Lopez-Molina et al., 2002; Borisjuk et al., 2004; Penfield et al., 2005). After germination, postgerminative growth is characterized by cotyledon opening, cotyledon greening, hypocotyl growth and radicle growth. Cotyledon greening marks the establishment of a seedling to become an autotrophic organism with photosynthetic capacity. In many cases, seed germination and subsequent postgerminative growth are collectively referred to as seed germination.

Seed germination and postgerminative growth are strictly regulated by phytohormones. In particular, abscisic acid (ABA) and gibberellin (GA) play predominant and antagonistic roles in the regulation of seed germination (Karssen et al., 1983; Olszewski et al., 2002; Kucera et al., 2005; Nambara and Marion-Poll, 2005). Whereas high GA/ABA ratio induces, low GA/ABA ratio inhibits seed germination (Karssen et al., 1983; Kucera et al., 2005). ABA is known to promote seed maturation and seed dormancy, but inhibit seed germination and postgerminative growth. The underpinning molecular mechanism of the ABA action during seed germination has been extensively studied. During the past two decades, genetic studies in Arabidopsis have identified many

aba-insensitive (abi) mutants using the germination assay, and several ABI genes have been characterized in some details (Koornneef et al., 1984; Giraudat et al., 1992; Finkelstein, 1994; Leung et al., 1994; Meyer et al., 1994; Finkelstein et al., 1998; Finkelstein and Lynch, 2000; Lopez-Molina and Chua, 2000; Lopez-Molina et al., 2001; Finkelstein et al., 2002). Among these ABI genes, ABI5 is one of the best-characterized genes. ABI5 encodes a basic leucine zipper (bZIP) transcription factor that acts as a key regulator of seed development and postgerminative growth (Finkelstein and Lynch, 2000; Lopez-Molina and Chua, 2000). Whereas the loss-of-function mutations in ABI5 cause the mutant insensitive to ABA (Koornneef et al., 1984; Finkelstein, 1994), the overexpression of ABI5 renders hypersensitivity to ABA during germination and postgerminative growth (Finkelstein and Lynch, 2000; Lopez-Molina and Chua, 2000). The transcription of ABI5 and the accumulation of ABI5 protein are highly enriched in developing and germinating seeds, and become rapidly decreased to the basal level shortly after seed germination (Lopez-Molina

et al., 2001). Moreover, the level of both ABI5 mRNA and ABI5 protein is positively regulated by ABA, correlated to the inhibitory effect of the phytohormone on seed germination and postgerminative growth, illustrating ABI5 as a key regulator in early seedling development (Lopez-Molina et al., 2001; Lopez-Molina et al., 2002). The stability of ABI5 protein is regulated by the proteasomal degradation pathway, involved in an E3 ubiquitin ligase KEEP ON GOING (KEG), which promotes ABI5 protein degradation (Stone et al., 2006; Liu and Stone, 2010). Moreover, DWA1 and DW A2 (DWD hypersensitive to ABA1 and 2), two substrate receptors of CUL4-DDB1-DWD (Cullin

4-Damaged DNA Binding1-DDB1 binding WD40) E3 ligase complexes, have also been shown to induce ABI5 degradation (Lee et al., 2010). A novel protein ABI FIVE BINDING PROTEIN (AFP) has also been reported to play a role in the regulation of ABI5 protein degradation (Lopez-Molina et al., 2003). AFP has also been proposed to connect ABI5 with a transcription repressor TOPLESS to repress the ABA response genes (Pauwels et al., 2010).

In addition to ABA and GA, cytokinin has been implied to play an important role in regulating seed germination (Barzilai and Mayer, 1964; Khan, 1971; Black et al., 1974; Thomas et al., 1997). Cytokinin is an essential phytohormone involved in the regulation of various aspects of plant growth and development, including seed germination (Werner and Schmülling, 2009). Cytokinin signaling is mediated by a two-component system-based phosphorelay, through which a phosphoryl group is sequentially transferred from the receptors to downstream components (Kakimoto, 2003; Müller and Sheen, 2007; To and Kieber, 2008; Hwang et al., 2012). I n Arabidopsis, three histidine kinases (HK), CYTOKININ RESPONSE1 (CRE1)/WOODEN LEG (WOL)/AHK4, AHK2 and AHK3 have been characterized as cytokinin receptors (Inoue et al., 2001; Yamada et al., 2001; Higuchi et al., 2004; Nishimura et al., 2004; Riefler et al., 2006). Downstream of the receptors, the phosphorelay consists of additional three major components, histidine phosphotransfer proteins (AHPs), type-B response regulators (ARRs), and type-A ARRs. AHPs accept a phosphoryl group from the cytokinin receptor, and then transfer to downstream type-B and type-A ARRs. Upon phosphorylation, type-B ARRs, a group of MYB-type transcription factors, are activated and directly promote the expression of cytokinin response genes, including type-A ARR genes. The expression of type-A ARR genes is highly inducible by cytokinin. Upon phosphorylation, type-A ARR proteins negatively regulate cytokinin signaling by unknown mechanisms, thereby forming a feedback regulatory loop (Müller and Sheen, 2007; To and Kieber, 2008; Hwang et al., 2012).

Recent studies indicate that the active crosstalk between ABA and cytokinin plays an important role in the regulation of the abiotic stress response (Ha et al., 2012). The homeostasis of cytokinin is controlled by two key enzymes. Whereas IPT (ISOPENTENYL TRANSFERASE) catalyzes the first rate-limiting step of cytokinin de novo synthesis, CKX (CYTOKININ OXIDASE) irreversibly degrades cytokinin (Sakakibara, 2006). The reduction of the cytokinin levels in the ipt multiple mutants or transgenic plants

overexpressing CKX causes a stress-tolerant phenotype (Nishiyama et al., 2011). Consistently, whereas the cytokinin level is decreased under the stress condition, many stress-related genes show an altered expression level in the ipt multiple mutants or by external application of cytokinins (Nishiyama et al., 2011; Nishiyama et al., 2012). Mutations in the cytokinin receptor genes or the overexpression of several type-A ARR genes also cause the tolerance to abiotic stresses (Tran et al., 2007; Shi et al., 2012). However, it remains largely unknown how the cytokinin signaling pathway perceives a stress signal (Ha et al., 2012). As an adaptation mechanism, the active crosstalk between cytokinin and ABA is also involved in the regulation of lateral root development by modulating the expression of ABI4 (Shkolnik-Inbar and Bar-Zvi, 2010).

It has long been proposed that cytokinin promotes seed germination, possibly by reverting the inhibitory role imposed by ABA and other factors (Khan, 1971; Black et al., 1974; Mok, 1994; Thomas et al., 1997; Davies, 2004). Note that, the term “seed germination” used in these studies referred to both seed germination and postgerminative growth. A recent study identified a gain-of-function mutant gim1 (germination insensitive to ABA mutants) that shows resistance to ABA during seed germination. GIM1 encodes an IPT (AtIPT8/PGA22), and the gim1/pga22 mutations cause a remarkably increased level of major cytokinin species (Sun et al., 2003; Wang et al., 2011). The antagonizing effect of cytokinin on ABA-inhibited seed germination was attributed to the cytokinin-repressed expression of ABI5 (Wang et al., 2011). However, the expression of ABI5 is only marginally regulated by cytokinin in an ABA-independent manner (Wang et al., 2011), indicating that the cytokinin-regulated ABI5 transcription is not a major regulatory mechanism. Instead, these observations suggest that an unidentified mechanism, rather than the transcription of ABI5, is employed to regulate the interaction between cytokinin and ABA. In this study, we show that cytokinin specifically antagonizes the ABA-mediated inhibition of cotyledon greening, a key developmental event during postgerminative growth. We demonstrate that cytokinin induces the degradation of ABI5 protein, thereby relieving germinating seedlings

from the inhibitory effect imposed by ABA.

RESULTS

Cytokinin promotes cotyledon greening by repressing the inhibitory effect of ABA Seed development and subsequent germination are regulated by several phytohormones, of which ABA promotes seed dormancy and inhibits seed germination. By contrast, cytokinin has been proposed to promote seed germination and postgerminative growth, possibly by antagonizing the ABA-mediated inhibitory effect (Khan, 1971; Wang et al., 2011). Note that, many previous studies collectively referred to seed germination and postgerminative growth as seed germination. When wild-type Arabidopsis (Columbia-0 or Col-0) seeds were germinated in the presence of ABA, the growth of the germinated embryos was arrested (Fig. 1A and 1B). As a marker of postgerminative growth and seedling establishment, cotyledon greening is strongly inhibited by ABA, with the complete inhibition by 0.5 μM ABA (Fig. 1C). Surprisingly, we found that cytokinin benzyladenine (BA) and 2-isopentenyladenine (2-ip) had no antagonizing effect on the inhibitory effect of ABA on seed germination (Fig. 1A and B, Supplemental Fig. S1). Instead, cytokinin antagonized the inhibitory effect of ABA on cotyledon greening during postgerminative growth in a dose-dependent manner (Fig. 1D and 1E, Supplemental Fig. S2). Notably, cytokinin reverted the ABA effect on cotyledon greening at lower concentrations (~ 0.5

μM), and the promotive effect of cytokinin was decreased at higher concentrations of cytokinin (Fig. 1F). To further confirm the effect of cytokinin on ABA during cotyledon greening, we analyzed the phenotype of pga22 that caused estradiol-induced overexpression of AtIPT8 and an elevated level of cytokinin (Sun et al., 2003). In the seed germination assay, the elevated level of cytokinin produced by overexpression of AtIPT8 had no obvious effect on seed germination and no antagonizing effect on the inhibitory

effect of ABA on seed germination (Supplemental Fig. S3A). However, the cotyledon greening rates were significantly increased in pga22 under 0.5 μM ABA and 10 μM estradiol treatments (Supplemental Fig S3B). These results indicate that cytokinin antagonizes the inhibitory effect of ABA on cotyledon greening with marginal effects on seed germination.

To further test whether cytokinin specifically antagonizes the inhibitory effect of ABA during early seedling establishment, we performed a similar experiment during the postgerminative growth stage. Wild-type seeds were stratified for 24 hrs, and the germinating seedlings were then transferred onto agar plates supplemented with 0.5 μM ABA in the presence or absence of cytokinin. Whereas ABA strongly inhibited cotyledon greening, cytokinin substantially reverted the inhibitory effect of ABA on cotyledon greening (Supplemental Fig. S4). Similarly, the osmotic stress (mimicked by mannitol) and salt stress (NaCl) also inhibited cotyledon greening, which was efficiently relieved by cytokinin (Supplemental Fig. S5). Taken together, these results suggest that cytokinin antagonizes the abiotic stress-mediated early growth arrest.

The cytokinin-relieved ABA inhibitory effect on cotyledon greening requires a functional cytokinin signaling pathway

To investigate whether the effect of cytokinin on ABA-inhibited cotyledon greening is dependent on the cytokinin signaling pathway, we first examined the cotyledon greening phenotype of the cytokinin-receptor mutants treated with cytokinin and ABA. In the presence of ABA, the ahk2-1 mutant showed a response to cytokinin similar to wild type (Fig. 2A), indicating that AHK2 does not play a major role in cytokinin-promoted cotyledon greening. However, the ahk3-1 and cre1-2 (an allele of ahk4) mutants displayed significantly reduced sensitivity to cytokinin when treated with both cytokinin and ABA. In particular, whereas nearly 80% of Col-0 cotyledons were turning green, less than 26% and 6% of ahk3-1 and cre1-2 mutant cotyledons became green, respectively (Fig. 2A). A similar

result was obtained by analyzing ahk4-1, an allele of cre1 in the Wassilewskija (Ws) background (Fig. 2A). We also examined the cotyledon greening phenotype of various combinations of the receptor gene double mutants. Compared with the single receptor gene mutants, all the three double mutants displayed the remarkably reduced sensitivity to cytokinin in the presence of ABA (Fig. 2A). These results indicate that the cytokinin receptors play redundant roles in antagonizing ABA during cotyledon greening, whereas AHK3 and CRE1/AHK4 play a more dominant role in this developmental process. Consistently, the expression of all three receptor genes was detected in germinating seedlings (Supplemental Fig. S6), and the predominantly expressed cytokinin receptor gene in developing embryos is CRE1/AHK4 (Müller and Sheen, 2008).

We next examined the possible involvement of the AHP genes in the crosstalk of cytokinin and ABA during the early growth arrest. Single mutations in any of the five AHP genes did not show an altered response to cytokinin in antagonizing the inhibitory effect of ABA on cotyledon greening (Fig. 2B), suggesting a high degree of genetic redundancy as revealed in previous studies (Hutchison et al., 2006; Deng et al., 2010). The ahp2-1,3,5-2 triple mutant is known to cause severely compromised response to cytokinin (Hutchison et al., 2006). Consistently, cytokinin-induced cotyledon greening was nearly completely lost in the ahp2-1,3,5-2 triple mutant (Fig. 2B), indicating that the genetic redundant AHP genes are functionally required for the cytokinin-mediated cotyledon greening. Collectively, the above results suggest that both the cytokinin receptors and AHPs are required for cytokinin-repressed ABA signaling during early seedling growth.

Cytokinin antagonizes ABA signaling mainly via ARR12

Type-B ARRs are transcription factors that act downstream of AHPs to positively regulate cytokinin signaling by directly promoting the transcription of type-A ARR genes. Of the 11 type-B ARR genes, ARR1, ARR10 and ARR12 play essential and redundant roles in the regulation of cytokinin signaling (Argyros et al., 2008; Ishida et al., 2008). We assumed

that cytokinin antagonizes the inhibitory effect of ABA through one or more of these three key type-B ARR genes. To test this possibility, we examined the response of the arr1-3,

arr10-5, arr12-1 and arr12-3 mutants to cytokinin in antagonizing ABA during cotyledon greening. We found that the arr1-3 and arr10-5 mutants showed a slightly reduced sensitivity to cytokinin in the cotyledon greening assay (Fig. 3A). However, two allelic mutants, arr12-1 and arr12-3, showed significantly reduced sensitivity to cytokinin in antagonizing the ABA effect (Fig. 3A). Notably, whereas arr12-1 was a null mutant allele, arr12-3 contained a T-DNA insertion in intron 2 and had residual expression of ARR12 (Supplemental Fig. S7A and S7B). Consistently, arr12-1 showed a stronger phenotype than arr12-3 in antagonizing the ABA effect in the presence of cytokinin (Fig. 3A). In a double mutant analysis, whereas the arr1-3 arr10-5 double mutant maintained approximately 35% of the activity, both the arr1-3 arr12-1 and arr10-5 arr12-1 double mutants were almost completely insensitive to cytokinin in the cotyledon greening assay (Fig. 3A). These results suggest that ARR12 plays an important role in cytokinin-regulated ABA signaling during cotyledon greening.

To further assess the specific role of ARR12 in antagonizing against ABA, we carried out an overexpression study. We generated two mutated transgenes ARR1ΔDDK-MYC and ARR12ΔDDK-MYC, in which the amino-terminal region encompassing the receiver domain (the DDK domain) was deleted. The receiver domain in type-B ARRs functions as a negative regulatory motif, and the removal of this region causes constitutive transcription activation in the absence of cytokinin (Sakai et al., 2001). These two transgenes were placed under the control of an estradiol-inducible promoter (Zuo et al., 2000), and then transformed into wild-type plants. The accumulation of the transgenic proteins was highly inducible by estradiol as assayed by protein blotting using an anti-MYC antibody (Fig. 3B). The transgenic seeds were germinated and grown on agar plates containing ABA and estradiol, and the cotyledon greening phenotype was scored. Under the assay condition, overexpression of ARR1ΔDDK had no detectable phenotype on antagonizing the inhibitory

effect of ABA in cotyledon greening (Fig. 3C). However, overexpression of ARR12ΔDDK remarkably increased the cotyledon greening rate in antagonizing the inhibitory effect of ABA, which was comparable to that in the wild-type seedlings treated with cytokinin (Fig. 3C). Moreover, the transgenic phenotype of the ARR12ΔDDK seedlings was correlated to the level of ARR12ΔDDK protein induced by estradiol (Fig. 3B and 3C). These results indicate that overexpression of ARR12ΔDDK is sufficient to activate the

cytokinin-mediated signaling events in promoting cotyledon greening.

Taken together, these results demonstrate that ARR12 plays a critical role to specifically repress ABA signaling during cotyledon greening.

Cytokinin induces proteasomal degradation of ABI5 protein

Given that cytokinin antagonizes ABA during cotyledon greening, we reasoned that cytokinin may target key signaling components of the ABA pathway. To identify the putative targets of cytokinin, we first examined the effect of cytokinin on the expression level of key ABA signaling components, including two SnRK2 genes (SnRK2.2 and

SnRK2.3), the ABF/AREB family genes (ABF1, ABF2, ABF3 and ABF4) and several ABI genes (ABI1, ABI2, ABI3, ABI4, ABI5 and ABI8). We found that cytokinin did not have substantial effects on the expression of these genes (see Supplemental Fig. S8). The expression level of most of the ABA-regulated genes remained largely unaltered by cytokinin (Supplemental Fig. S8). The ABA-induced expression of ABI5 was slightly reduced by cytokinin (Supplemental Fig. S8; reduced approximately 1.3-fold by cytokinin), similar to that observed in a previous study (Wang et al., 2011).

ABI5 is key regulator involved in ABA-regulated seed germination and postgerminative growth, whereas the accumulation of the ABI5 transcript and ABI5 protein is positively regulated by ABA (Lopez-Molina et al., 2001; Stone et al., 2006). Since cytokinin had marginal effects on the transcription of ABI5 (Wang et al., 2011) (see also Supplemental Fig. S8), we then examined whether the stability of ABI5 protein is regulated

by cytokinin. Because ABI5 protein is rarely detectable following germination and is significantly induced by ABA in a narrow developmental window (Lopez-Molina et al., 2001), we analyzed the accumulation of ABI5 protein in germinating seedlings treated with various combinations of ABA and cytokinin, following a similar approach as described (Lopez-Molina et al., 2001). The wild-type seeds stratified in the absence of ABA were transferred to agar plates supplemented with various combinations of ABA and cytokinin, and then cultured for different times. Under the assay condition, ABI5 protein was strongly induced by ABA as previously reported (Lopez-Molina et al., 2001), but barely detectable in the untreated samples at all the tested time intervals (Fig. 4A). Strikingly, the

ABA-induced accumulation of ABI5 protein was efficiently reduced by cytokinin, and reached at an undetectable level 96 hrs post-stratification (Fig. 4A). Notably, the cytokinin-induced reduction of ABI5 protein was reversed by MG132 (Fig. 4B), an inhibitor specific to the proteasomal degradation machinery. This result suggests that cytokinin-regulated reduced accumulation of ABI5 is mediated by the 26S proteasomal pathway, presumably by a similar mechanism as previously reported (Lopez-Molina et al., 2001; Lopez-Molina et al., 2003; Stone et al., 2006; Liu and Stone, 2010).

We also analyzed the stability of HA-ABI5 protein in the 35S:HA-ABI5 transgenic plants (Lopez-Molina et al., 2001). Similar to that observed in germinating seeds, the accumulation of HA-ABI5 protein was induced by ABA, but was dramatically reduced by cytokinin in 8-day-old seedlings (Fig. 4C), indicating that cytokinin also promotes ABI5 degradation in the established young seedlings. Consistently, overexpression of ABI5

(35S:HA-ABI5) nearly abolished the sensitivity to cytokinin during cotyledon greening (Supplemental Fig. S9), correlated to the accumulation of a higher level of HA-ABI5 protein in the transgenics (Fig. 4C). It should be noticed that the stability of other ABA signaling proteins may also be regulated by cytokinin, and it will be interesting to investigate the possible regulatory mechanism upon the available of specific antibodies recognizing these proteins.

Involvement of the cytokinin signaling components in the cytokinin-induced degradation of ABI5

Data presented above indicate that cytokinin induces the degradation of ABI5, correlated to the cytokinin-promoted cotyledon greening that requires the cytokinin signaling components, mainly including CRE1/AHK4, AHP2, 3, 5 and ARR12. We next examined whether these cytokinin signaling components are also involved in the regulation of ABI5 degradation. Whereas the ABA-induced accumulation of ABI5 protein was completely degraded in ahk2-1 in the presence of cytokinin, a phenotype similar to that in the wild-type seeds, the residual level of ABI5 remained in ahk3-1 (Fig. 5A). In the ahk4-1 mutant, however, the cytokinin-induced degradation of ABI5 was nearly abolished (Fig. 5A), indicating that cytokinin-induced ABI5 degradation is mainly dependent on CRE1/AHK4, which is predominantly involved in the cytokinin-antagonized effect against ABA during early seedling growth. Similarly, whereas ahp2-1, ahp3, and ahp5-2 showed a

wild-type-like phenotype in response to cytokinin, ahp2-1,3,5-2 rendered the triple mutant insensitive to cytokinin in the regulation of ABI5 degradation (Fig. 5B).

In the analysis of the regulatory role of ARR1, ARR10 and ARR12, we found that the cytokinin-induced degradation of ABI5 protein in arr1-3 and arr10-5 were similar to that in wild type, but was substantially blocked in arr12-1 (Fig. 5C). Compared to that of the

arr12 single mutants, a stronger phenotype was observed in the arr1-3 arr12-1 and arr10-5 arr12-1 double mutants, in which the accumulation of ABI5 protein was nearly not affected by cytokinin (Fig. 5D). Conversely, estradiol-induced overexpression of ARR12ΔDDK enhanced the degradation of ABI5 protein (Fig. 5E). Previous studies have shown that ARR4, ARR5 and ARR6 are involved in the cytokinin-ABA interaction during seed germination (Wang et al., 2011). Analysis of the accumulation of ABI5 protein in the

arr3,4,5,6 quadruple mutant revealed that the cytokinin-induced ABI5 protein degradation was dramatically reduced in arr3,4,5,6 (Supplemental Fig. S10), indicating that these

type-A ARR genes also play an important role during cotyledon greening.

Taken together, the above results indicate that key components in the cytokinin pathway are functionally required for the cytokinin-regulated ABI5 protein degradation, correlated to the observation that these components are also predominantly involved in the cytokinin-antagonized effect against ABA during early seedling growth.

ARR12 functions upstream of ABI5 to regulate cotyledon greening

The observation that cytokinin antagonizes the ABA effect on cotyledon greening and promote the degradation of ABI5 protein implies possible genetic interactions between cytokinin signaling and ABI5. To test this hypothesis, we performed a double mutant analysis by crossing abi5-8 and arr12-3, both of which are in the Col-0 background. The abi5-8 mutant is a weak allele containing the detectable level of ABI5 protein (Zheng et al., 2012) (Supplemental Fig. S11), and showed a partial insensitive phenotype to ABA during cotyledon greening (Fig. 6A and 6B). In the presence of cytokinin, abi5-8 showed significantly reduced sensitivity to ABA. Under all assay conditions, the abi5-8 arr12-3 double mutant showed an abi5-8-like phenotype. In particular, the abi5-8 arr12-3 double mutant showed an abi5-8-like phenotype in the presence of both ABA and cytokinin (Fig

6A and 6B). These results suggest that ARR12 genetically acts upstream of ABI5 to promote cotyledon greening.

DISCUSSION

In this study, we have used multiple approaches to define a genetic pathway that integrates a cytokinin signal into the ABA-mediated early seedling establishment. This pathway mainly consists of the cytokinin receptors AHK3 and CRE1/AHK4, multiple AHP genes (AHP2, 3 and 5), ARR12 and ABI5. We also demonstrate that ABI5, a key transcription

factor gene in the ABA signaling pathway, acts downstream of the cytokinin pathway to transduce a cytokinin signal during early seedling growth. Biochemically, we show that cytokinin negatively regulates the stability of ABI5 protein to modulate ABA signaling. These findings reveal an important mechanism that integrates cytokinin signaling and ABA signaling to coordinate plant growth and development.

Seed germination is a complex process initiated with the uptake of water by the quiescent dry seed and terminated with the elongation of the embryonic axis. The key developmental event during post germinative growth is the establishment of a seedling, involved in the mobilization of the major storage reserves and, morphologically, is featured by cotyledon opening, cotyledon greening and radicle growth (Bewley, 1994). Both seed germination and early seedling establishment are under the tight control of the genetic programs and the environmental factors. It has been well recognized that ABA plays a vital role by repressing seed germination and subsequent early seedling establishment, of which ABI5 is an important regulator of these developmental processes (Finkelstein and Lynch, 2000; Lopez-Molina and Chua, 2000; Lopez-Molina et al., 2001; Lopez-Molina et al., 2002). In addition, cytokinin has been proposed to play positive roles in regulating seed germination, possibly through antagonizing against the effect imposed by ABA (Khan, 1971; Wang et al., 2011). Unexpectedly, we found that cytokinin is not required for antagonizing the ABA effect during seed germination. Instead, cytokinin plays an important role in early seedling establishment, in particular, cotyledon greening, by antagonizing the inhibitory effect of ABA. Consistently, a major physiological role of cytokinin is to promote plastid differentiation and other photomorphogenesis processes (Chory et al., 1991; Chory et al., 1994; Thomas et al., 1997), which marks the transition from heterotrophic to autotrophic growth of a seedling during early growth. Additionally, both the cytokinin receptor genes and AHP genes are involved in the far red light-regulated seed germination (Hutchison et al., 2006; Riefler et al., 2006). Therefore, the cytokinin-repressed ABA signaling, particular during postgerminative growth, represents an important regulatory

mechanism to coordinate early seedling establishment.

The bZIP transcription factor ABI5 has been shown as a key regulator during seed germination and postgerminative growth (Lopez-Molina et al., 2001; Lopez-Molina et al., 2002). The steady level of ABI5 mRNA and the accumulation of ABI5 proteins are positively regulated by ABA, thereby forming a positive feedback regulatory loop that acts to monitor the environmental changes during seed germination and postgerminative growth (Lopez-Molina et al., 2001). Considering that both the ABI5 transcript and ABI5 protein are rapidly turned over shortly after seed germination (Lopez-Molina et al., 2001), it is reasonable to presume that the promoting effect of cytokinin on cotyledon greening is likely linked to the cytokinin-regulated ABI5 abundance at the transcriptional or posttranscriptional level. Whereas the ABI5 transcription is not regulated by cytokinin, the ABA-promoted ABI5 transcription is slightly reduced by cytokinin (Wang et al., 2011) (see also Supplemental Fig. S7). Moreover, we noticed that cytokinin slightly represses the

ABA-induced ABI5 expression (Wang et al., 2011) (Supplemental Fig. S7), indicating that the cytokinin-repressed ABA signaling is not executed by the regulation of the transcription of ABI5. Instead, an alternative mechanism, rather than the cytokinin-repressed ABI5 mRNA level, may play a more dominant role in regulating the ABI5 activity. In agreement with this notion, we found that cytokinin efficiently induces the degradation of ABI5 protein. Intriguingly, treatment with cytokinin for 72-96 hr results in nearly complete degradation of ABI5 protein with a moderately reduced level of ABI5 mRNA under the assay condition, suggesting that the stability of ABI5 protein, rather than the steady level of ABI5 mRNA, is the major regulatory step of the cytokinin-mediated ABA signaling. Genetically, cytokinin-induced degradation of ABI5 protein is tightly coupled with the antagonizing effect of cytokinin on ABA signaling, mainly involved in CRE1/AHK4, AHP2, 3, 5 and ARR12, further indicating that cytokinin represses ABA signaling by modulating the stability of ABI5 protein during early seedling growth. Given that ARR12 plays an important role in the regulation of cytokinin-induced ABI5 degradation, an apparent

challenge is to fill the gap between ARR12 and ABI5. Notably, ABI5 physically interacts with ARR4, 5 and 6 (Wang et al., 2011), three type-A ARRs that act downstream of type-B ARRs. The observation that the cytokinin-induced ABI5 degradation is reduced in the

arr3,4,5,6 quadruple mutant implies that the binding of type-A ARR proteins to ABI5 may play an important role in regulating the stability of ABI5 protein. Because both the steady level of type-A ARR mRNA and the accumulation of type-A ARR proteins are positively regulated by cytokinin (Brandstatter and Kieber, 1998; Imamura et al., 1998; To et al., 2007; Ren et al., 2009), it is likely that the type-A ARR-ABI5 complex may inhibit ABI5 protein to interact with the proteasomal degradation machinery.

In addition to its regulatory role in seed germination and postgerminative growth, the ABA-cytokinin interaction has also been implied in the regulation of stress responses (Ha

et al., 2012). Whereas abiotic stresses cause the reduction of the cytokinin level, the reduced cytokinin level, in turn, results in the resistance to salts and drought (Nishiyama et al., 2011). Notably, several key signaling components in the cytokinin pathway have been shown to negatively regulate the stress response (Tran et al., 2007; Shi et al., 2012), indicating that cytokinin-repressed ABA signaling operates not only in seed germination and seedling establishment, but also persistent in the stress response. Collectively, these discoveries reveal that cytokinin negatively regulates ABA-mediated stress responses, in particular by promoting ABI5 degradation during early seedling growth, thus illustrating an important mechanism for adaptation growth of plants in response to various internal and environmental signals.

MATERIALS AND METHODS

Plant materials and growth conditions

The Col-0, Ws and L er wild type strains were used in this study. The ahk4-1 and abi5-4 mutants were in the Ws background, and all other mutants were in the Col-0 background. The mutants (pga22, ahk2-1, ahk3-1, ahk4-1, ahk2-5 ahk3-7, ahk2-5 cre1-2, ahk3-7 cre1-2, ahp1, ahp2-1, ahp3, ahp4-1, ahp5-2, arr1-3, arr10-5, arr12-1, abi5-4, abi5-8 and

arr3,4,5,6) (Lopez-Molina and Chua, 2000; Inoue et al., 2001; Alonso et al., 2003;

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Seeds were surface sterilized with 10% (v/v) bleach, and then sowed on GM medium (1X Murashige and Skoog salts, 1% sucrose, 1 X B5 vitamin, 0.05% MES-KOH, and 0.3% Phytagel). Unless otherwise specified, the plates were kept for 2 days in the dark at 4o C (stratification), and then transferred into a tissue culture room under constant white light (100 μmoles m-2 s-1) at 22o C.

Agrobacterium tumefaciens-mediated transformation of Arabidopsis plants was performed by the floral dip method (Bechtold and Pelletier, 1998). The agrobacterial strain GV3101 was used in all transformation experiments.

Seed germination assay and cotyledon greening assay

The same batches of seeds of various genotypes grown under the same conditions were used in all experiments for the seed germination assay and the cotyledon greening assay. After 2 days of stratification at 4o C, seeds were transferred to a tissue culture room. Seed

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对开放课堂教学管理系统建设内容进行分析建模。系统合理规划，功能完善，方便师生共同使用，减少相关工作人员的工作量；实现学习空间上的资源共享，激发学习者的学习动机，学生完成社会性交互，促进学生主动参与，提升学习效果；学习空间管理方面，减轻管理员工作，采用信息系统的管理模式，学习空间主要实现项目课程的安排，师生通过访问服务器可以方便地查询、提交有关教学资源。 二、系统结构 系统根据教学需求把用户分为四类，有教师用户、学生用户、系统管理员用户、学习空间管理员用户。针对具体的用户，系统根据用户数据库提供的信息设置相应的权限和功能。学生使用这个系统可以运用个人密码登录，然后在线查看课程安排时间、地点，浏览工作项目信息，提交项目报告，修改个人信息，评定其他学生的工作项目，查看自己项目课程成绩；教学一线的教师登录这个系统主要是查询本人授课的班级，所在的地点、时间，评定学生学习空间平时的课程成绩，跟踪学生的互动信息，记录学生在开放课堂的表现，修改个人资料，申请使用学习空间并查看结果，申请设备，发布及管理项目报告资源；学习空间的管理人员登录系统进行学习空间项目信息管理，管理耗材信息，管理设备信息，检索并分配学习空间，审核学习空间申请，查看学习空间申请及学习空间安排；系统管理员登录本系统设置学习空间、

网络教学管理系统的主要功能

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教务管理系统课程设计报告

教务综合管理系统设计报告 专业：软件工程 成员：车振军陆建伟 徐蕾杨思倩 指导老师：徐明 日期：2016-6-15

一、引言 目的 为了保证项目小组能够按时完成小组任务及目标，便于项目小组成员更好地了解项目情况，使项目小组开展的各个过程合理有序，因此确定各个项目模块的开发情况和主要的负责人，供各项目模块的负责人阅读，做到及时协调，按步有序进行项目的开发，减少开发中的不必要损失。 预期的读者是设计人员、开发人员、项目管理人员、测试人员和用户。 背景 高校教务管理工作是高等教育中的一个极为重要的环节，是整个院校管理的核心和基础。面对种类繁多的数据和报表，手工处理方式已经很难跟上现代化管理的步伐，随着计算机及通讯技术的飞速发展，高等教育对教务管理工作提出了更高的要求。尽快改变传统的管理模式，运用现代化手段进行科学管理，已经成为整个教育系统亟待解决的课题之一。 教务管理系统是一个大型复杂的计算机网络信息系统，满足各类高校现在和将来对信息资源采集、存储、处理、组织、管理和利用的需求，实现信息资源的高度集成与共享，实现信息资源的集中管理和统一调度。为各级决策管理部门提出准确、及时的相关信息和快捷、方便、科学的决策分析处理系统；为信息交流、教务管理提供一个高效快捷的电子化手段；最终达到进一步提高各级领导科学决策水平，提高各院系、各部门管理人员管理水平与办公效率，减轻工作负担的目的。 教务管理系统面向管理员、教师和全校学生，实现学生管理、教师管理、课程管理、成绩处理。 定义 MySQL MySQL是一个关系型数据库管理系统，由瑞典MySQL AB 公司开发，目前属于 Oracle 旗下公司。MySQL是一种关联数据库管理系统，关联数据库将数据保存在不同的表中，而不是将所有数据放在一个大仓库内，这样就增加了速度并提高了灵活性。 MySQL所使用的 SQL 语言是用于访问数据库的最常用标准化语言。MySQL 软件采用了双授权政策，它分为社区版和商业版，由于其体积小、速度快、总体拥有成本低，尤其是开放源码这一特点，一般中小型网站的开发都选择 MySQL 作为网站数据库。

教务管理系统软件工程课程设计

教务管理系统软件工程课程设计

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（5）启动探究性学习活动，增强教学竞争力与吸引力。（6）积极推进课题研究，以科研指导教研。 4、努力创新，争取“人无我有，人有我优，人优我特”，力争教师有特点，学生有特长，学校有特色。创办精品名校，以省市级重点名校为参照系，按照师资一流、管理一流、质量一流设施一流的标准,建设具备多方面可持续发展条件的、高起点高品位、高质量的学校，全市著名的中华名校。创办精品名校的深远意义在于：第一，通过它可以树立起学校别具特色、别具优势、别具魅力的教育品牌；第二，通过名校效应，整合本校的优质教育资源，为本市教育事业作贡献。

课堂教学管理有哪些功能

课堂教学管理有哪些功能？ 课堂是学生学习的场所。课堂教学是教育教学中普遍使用的一种手段，它是教师传授学生知识和技能的全过程。学生是学习的主体，是学习的主人。在教学中，教师应该根据教学实际，运用自己的智慧和创造力，创设必要的情境，让学生在特定的环境中进行实践体验，把课堂营造成生动活泼的学习乐园，让学生在愉快的学习环境中自然、有序地学习。使他们在活动中感悟道理，体验情感，规范行为。 教学组织形式所要解决的问题，就是教师以什么样的形式将学生组织起来，通过什么样的形式与学生发生联系，教学活动按照什么样的程序展开，教学时间如何分配和安排等问题。教学组织形式对于教学活动的质量和效果具有非常重要的影响，在教学的其他方面相同的情况下，教学组织形式的不同会带来极为不同的教学效果。矚慫润厲钐瘗睞枥庑赖賃軔朧碍鳝绢。 矚慫润厲钐瘗睞枥庑赖賃軔朧碍鳝绢。 课堂教学管理是教师为了完成教学任务，调控人际关系，构建教学环境，引导学生学习的一系列教学行为方式。管理好课堂是开展教学活动的基石，教师必须不断地提高课堂教学管理 技能。聞創沟燴鐺險爱氇谴净祸測樅锯鳗鲮。聞創沟燴鐺險爱氇谴净祸測樅锯鳗鲮。 ( 一) 组织功能是课堂管理最基本的功能。课堂教学的有效进行，依赖于教师对教学设备、 教材、学生以及教学活动进行有效的组织，这样，学生才能由分散的个体变成有效的学习集体，教材、教学设备才能充分发挥作用，教学活动才能系统、有序地进行。残骛楼諍锩瀨濟 溆塹籟婭骒東戇鳖納。残骛楼諍锩瀨濟溆塹籟婭骒東戇鳖納。 ( 二) 促进功能是指良好的课堂管理可以最大限度地满足课堂中学生个体和集体的合理需 要，形成积极、和谐的课堂学习环境，激励学生的参与精神，激发学生的潜能释放，促进教 学活动的顺利进行，提高教学效率。酽锕极額閉镇桧猪訣锥顧荭钯詢鳕驄。酽锕极額閉镇桧猪訣锥顧荭钯詢鳕驄。 ( 三) 协调功能是由课堂管理对象的特点决定的。由于课堂是由人、物、信息、时间等要 素组成的复杂系统，就其中的主要因素人来说，几十个学生在一起活动，没有行动上的协调一致，教学就无法进行。要发挥课堂系统的整体功能，取得良好的教学效果，必须充分发挥 课堂管理的协调功能。彈贸摄尔霁毙攬砖卤庑诒尔肤亿鳔简。彈贸摄尔霁毙攬砖卤庑诒尔肤亿鳔简。( 四) 维持功能是指教师通过一定的管理手段，较持久地维持课堂教学的基本秩序以形成 比较稳定的教学环境，保证教学活动的顺利进行。謀荞抟箧飆鐸怼类蒋薔點鉍杂篓鳐驱。謀荞抟箧飆鐸怼类蒋薔點鉍杂篓鳐驱。 课堂教学组织与管理的类型特点 ( 一) 放任型 教师的课堂教学组织与管理意识淡薄，工作责任心较差，他们在课堂上表现为只顾讲课，不顾效果，放任自由。对于学生在学习过程中出现的问题漠不关心，也没有积极的课堂管理要求。学生表面上乐得自在，实际上求知需要得不到满足，往往产生对教师的不尊重，学习动 机不足，学习热情不高，教学效果很差。初中生物学科是学生、家长和学校都相对不太重视 的小学科，许多教师也因此放任自流，应付差事，不利于学生对生物学知识体系的初步构建， 不能为高中学习奠定扎实的基础，也没有培养出对生物学科学习的兴趣和动力。厦礴恳蹒骈時盡继價骚卺癩龔长鳏檷。厦礴恳蹒骈時盡继價骚卺癩龔长鳏檷。 ( 二) 独断型 教师对学生的课堂表现要求严厉，但这种要求往往只根据教师个人的主观好恶确定，忽视学生自身的学习特点和教学目标的具体要求。在独断型管理的课堂上，学生的意见得不到充分发表，且学生往往有一种紧张感、压抑感，容易导致课堂管理的形式主义倾向，教学效果一 般。这样的教学组织与管理方式，不利于那些概念性较强或较抽象枯燥的生物学知识的学习。 茕桢广鳓鯡选块网羈泪镀齐鈞摟鳎饗。茕桢广鳓鯡选块网羈泪镀齐鈞摟鳎饗。 1 / 2

教学管理系统

教学管理系统数据库的设计 一．研究背景 Microsoft Access是现今最为流行的桌面数据库管理系统之一，可以满足各种信息管理的需要。它具有界面好、操作简易快捷、功能强大、接口灵活等特点。应用Access 开发的教学管理软件，界面简洁，操作简单，运行速度快，相比较堆集Word或Excel文档的管理模式大幅提高信息提取及信息处理效率。Access被应用于许多企业以及行政事业单位中，它与office的其他组件的无缝联结更让它在各行业应用中的地位得以提高。 在Access数据库中有7种不同类型的对象，即表、查询、窗体、报表、数据访问页、宏和模块，不同的对象在数据库中起着不同的作用，表用来存储数据；查询对数据库进行查看和分析；窗体可为数据库的控制、数据的输入、显示查询数据等操作设置友好的外观；报表以格式化的形式来对外展示数据；数据访问页将数据制作成WEB页，使之可以发布到互联网上；宏将自动完成一个或一组操作；模块能自动完成常规任务并创建业务解决方案。表是数据库的核心与基础，存放着数据库中的全部数据。报表、查询和窗体都是从数据表中获得数据信息，以实现用用户的某一特定的需求，通过窗体可以直接或间接地调用宏或模块，并执行查询、打印、预览、计算等功能，甚至可以对数据库进行编辑修改。 本文所设计的数据库，即是基于这种Acess软件下设计的系统，高校教学管理工作是一项复杂的系统工程，有其完整的系统概念体系和系统体系结构，目前的教学管理方式已严重阻碍了高等教育的深化改革和教学质量的进一步提高，更不适应二十一世纪培养人才的需要。实现教学管理系统网络化的首要工作应该是规划和创建可共享的数据库，即通过全面的收集、分析教务处各业务部门所用的大量数据，设计、优化并统一格式，生成适用于教学网络化管理的数据库结构，集中在数据库服务器上存储、管理与维护，实现数据在各用户间安全可靠和正确有效的流通，达到数据共享。 教学管理系统主要实现对一般高校的的教学工作的信息化管理。本系统实现了对教师的基本信息和教师的授课信息的登记、统计和查询等功能。类似的还对学生的基本档案信息、学习成绩信息进行保存、统计和查询。同时实现了对课程信息和学生选课信息的管理。本系统很大程度地实现了学校教学工作的信息化管理。 二．需求分析 1．系统需求分析 教学管理系统从功能来说，主要是实现对一般高校的信息化管理系统。用户的需求可分为如下3个方面： （1）教学管理人员通过该系统登录学生、教师和课程的有关信息。

谈谈如何进行有效地课堂教学的管理系统

谈谈如何进行有效的课堂教学管理 周载理 在课堂教学中，教师如果管理不好，就会影响学生的听课，影响教学效率的发挥。教师应具备进行有效的课堂管理能力，只有这样，才能在学生学习活动中起着引导者、促进者的作用，如何进行有效的课堂管理，以下是本人一些粗浅看法。 一、认真备课、精心设计 在教学过程中，认真备课，这是课堂有效管理的前奏；精心设计教学内容，将最新的教学理念融入到每节课的教学过程中，激发学生的求知欲和兴趣。有效的备课有利于教师落实地教、巧妙地教，促进学生学得快、学得扎实。40时间的分配和控制，切不可前紧后松。甚至拖堂是不可取的。. 二、让学生自我管理 当课堂教学已能充分发挥学生主体作用和教师主导作用时，学生良好的学习习惯和风气基本养成，自控力、自制力都大大提高，这时可由学生自我管理。"管"是为了达到不管，这是我们课堂教学管理的最高境界。这时教师重在指导学生管理的方法和经验，使他们学会管理。同时加大教学改革力度，采用各种方式，. 三、关注每位学生。 在平时的课堂上，教师更要关注每位学生，要走到学生中去，看学生是否在听课。教师从学生的眼神中了解真实的东西。眼睛

是心灵的窗户。教师要善于从学生的表情变化中看出自己的教学效果，辨析学生听讲的状况。教师课堂上视野所及，可以眉目传情，促进学生专心听讲。偶尔有学生面朝窗外，思想"跑马"，教师可运用目光注视，将自己的愿望迅速传递给学生。淡漠、严厉、责备的目光使学生触目知错，立即醒悟；热情、慈祥、赞许的目光使学生触目会意，精神振奋。教师不论是提出问题、指导自学、启发释疑或小结强化，都要用期待的目光，尽可能去平视或环顾大多数，切不可老是两手扶案，目无学生。也不能只站在教室一隅，视线顾此失彼。尤其要不时地环视教室前后左右，特别是后排的左右两角，对潜能生，更应予以满腔热情的关注每一学生。。 课堂有效管理方式方法多样。只有学生的实际情况，实施有效课堂管理，才能提高教学效果。

学校教务管理系统--数据库课程设计

学校教务管理系统 I.需求分析： 随着学校的规模不断扩大，学生数量急剧增加，有关学生的各种信息量也成倍增长。面对庞大的信息量，就需要有学生教务信息管理系统来提高学生管理工作的效率。通过这样的系统，可以做到信息的规范管理、科学统计和快速的查询，从而减少管理方面的工作量。 学校为方便教务管理，需开发一个教务管理系统。为便于学生，老师，教务管理人员信息查询，注册以及信息修改，学校把学生的信息，包括姓名、性别、年龄，成绩等信息输入教务管理系统的数据库，然后在管理终端可以对数据进行查询和修改操作。 要求系统能有效、快速、安全、可靠和无误的完成上述操作。并要求系统界面要简单明了，易于操作，程序利于维护。 一、信息分析： （1）学校教务管理的数据库，包含以下信息： 学校有若干个系，每个系有若干名教师和学生，每个教师可以担任若干门课程，并参加多个项目，每个学生可以同时选修多门课程，每门课程每学期可能有多名教师教授，课程分为必修、选修、任选三种。 （2）学校的教务管理的信息包括：

学生姓名、学号、班级、性别、班号，籍贯、出生日期、所属系编号、所属系名称、系主任，教师编号，教师姓名，教师职称，教师所授课程、课程编号，课程名，课程学分，项目编号，项目名称，项目负责人，学生选修课程及成绩。学生如果课程及格，可以取得该课程的学分。学生的各类型课程学分和总学分累计到一定程度，学生可以毕业。根据成绩高低，可以计算学分积。及格学生的学分积公式：课程学分积＝（该课程成绩－50）/10×该课程学分。 二、功能分析： （1）用户能够使用友好的图形用户界面实现对系、班级、学生、教师、课程、选课等内容进行增、删、改，以及对信息的 查询。对于查询要实现比较强大的功能，包括精确查询、 模糊查询以及统计查询。 （2）具体查询在数据库中要实现以下的功能： 1)所有来自某省的男生 2)所有某课程成绩>90的同学 3)教授某课程的老师 4)某班年龄最大的5名同学 5)某年以后出生的男同学 6)选修某课程的学生及其成绩 7)没有授课的教师 8)某学生所选课程的总学分 9)教授某学生必修课程的老师情况

教务管理系统(软件工程课程设计)

软件工程实践报告 教务管理系统 第一章问题定义 随着学校规模的扩大，人员的不断增加、复杂程度逐渐增强，学校中，教务是一项繁琐的事，每年都有新生入学、老生毕业，以及其他各种人事变动。每学期的考试成绩都需要分析，纵、横向比较，能及时反馈信息，还要对教师的教学成绩考核提供数据。如何有效地管理、分析、处理这些信息，帮助学校和教师掌握学生的情况，这就是教学信息管理系统需要完成的功能。以前简单的用Excel来打印几张报表的人机作坊再也无法适应当今学校的教学管理了，比如用Excel虽然能简单管理学生的学籍、成绩等，但用户界面简单，管理起来难度大，修改和查找学生的信息都比较麻烦，并且在操作过程中没有用户权限，只要能打开计算机的人就能打开数据进行任意的修改，大大的降低了信息的安全性和保密性,效率低,,人工的大量浪费；另外时间一长,将产生大量的文件和数据,这对于查找、更新和维护都带来了不少困难。随着科学技术的不断提高,计算机科学日渐成熟,其强大的功能已为人们深刻认识,它已进入各个领域并发挥着来越重要的作用。 作为计算机应用的一部分,使用计算机对学校的各类信息进行管理,具有着手工管理所无法比拟的优点.例如:检索迅速、查询方便、效率高、可靠性好、存储量大、保密性好、寿命长、成本低等。这些优点能够极大地提高学校信息管理的效率。

1．1问题定义 1．所需资源： 硬盘>80G，内存>256，处理器一般以上水平即可。 2.系统名为：教务管理系统 （1），本处理的信息主要有三大类：学生信息、教师信息、成绩数据。本系统主要着手于以上三大部分，建立数据库以及对数据的各种操作功能。 对于学生信息，由于需要经常性地进行各种查询。例如：查询一个班级中团员的人数，男女生的人数等等。教导处在每一届学生进校时必须进行分班，设置学号；每一届学生毕业，要进行学生信息备份； 对于教师信息，学校教导处跟据老师所教班的成绩对教师的成绩成行考核，可以进行同科的纵横向比较。（由于对教师方面不太了解只有这些） 对于成绩管理，课任教师要进行本科目成绩登记，计算平均分、优秀率、及格率；教导处要分段统计学生人数及所占比列，每学期进行学生成绩备份；学校领导则可通过查询工具来了解学生成绩情况。 （2），以上各类信息目前还处于手工或半手工的管理状态，效率低，可靠性差。如果采用计算机进行以上各类信息的管理，必将大大提高工作效率，对各类信息的维护及了解起到积极的作用。因此一个功能完备的学校信息管理系统的开发都非常有必要。 第二章可行性研究 2．1系统概述 本系统将采用面向对象的软件开发方法，以SQL 2000作为后台数据库，配合功能强大的SQL查询语句，用Delphi便捷地开发教学管理信息系统的应用程序。 2．2．1可行性分析 A 技术可行性：对Delphi能够运用自如，对SQL语句熟练掌握运用。 B 经济可行性：开发费用合理 C 操作可行性：能够良好的解决用户需要的问题

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