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75 Integrating Membrane Transport with Male Gametophyte ... - TAIR

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199 The Trichome Pock Phenotype of agb1 and pom1<br />

Zachary Larson-Rabin, Christopher Day<br />

University of Wisconsin-Madison<br />

Socket cells, which are specialized epidermal cells surrounding the base of Arabidopsis trichomes, differentiate<br />

following an unknown recruitment mechanism. These cells, numbering twelve on average in wild-type Columbia, serve<br />

to support the trichome. We have identified two mutants characterized by trichome pocks, which are deep indentations<br />

of the leaf surface at the base of some trichomes. The pocks correlate <strong>with</strong> an increase in socket cell number.<br />

We have mapped one mutant and found that it has a loss-of-function mutation in AGB1, the beta subunit of the<br />

heterotrimeric G-protein complex. Some of the pleiotropic phenotypes of the agb1 mutant have been described before,<br />

and include auxin and ABA hypersensitivity, erecta-like aerial defects, and root morphology and growth alterations. In<br />

this poster, we will describe the undocumented trichome pock phenotype of agb1.<br />

Another mutant that exhibits the trichome pock phenotype is the erh2 allele of POM-POM1 (POM1/ERH2/ELP1/<br />

AtCTL1). Trichomes of the erh2 allele show extra socket cells, sometimes as many as 30 per trichome. These plants also<br />

have root morphology phenotypes similar to agb1. In addition, stomata often form between socket cells or even adjacent<br />

to trichomes. This is not seen in wild-type or in agb1, in which stomata always form outside the socket cell zone. The<br />

gene product of POM1, a chitinase-like protein, has been implicated in repressing ethylene production and signaling.<br />

Our poster will describe our characterization of the trichome pock phenomenon, <strong>with</strong> regard to possible intercellular<br />

signals that control socket cell number.<br />

200 Adenosine Kinase Deficient Lines Display Abnormal Development<br />

Sarah Schoor 1 , Katja Engel 1 , Filomena Ng 1 , Sanghyun Lee 1 , Neil Emery 2 , Barb Moffatt 1<br />

1<br />

Univeristy of Waterloo, Waterloo Ontario, Canada, 2 Trent Univeristy, Peterborough Ontario, Canada<br />

By recycling adenosine into AMP, adenosine kinase (ADK; EC 2.7.1.20) plays a key role in maintaining nucleotide<br />

pools and methylation. In Arabidopsis, ADK is represented by two highly similar isoforms, ADK1 (At3g09820) and ADK2<br />

(At5g03300). Aside from establishing that ADK1 is expressed at higher levels than ADK2 throughout Arabidopsis, no<br />

distinct role has been assigned to either isoform. In order to establish the roles of these isoforms, as well as ADK activity<br />

itself, gene silencing lines (sADK) and T-DNA mutants lacking either ADK1 or ADK2 were identified. The metabolism<br />

and development of these mutants were then examined by establishing their remaining ADK activity and documenting<br />

their corresponding growth rate, leaf and meristem development and DNA methylation using HPLC analysis. The results<br />

indicate no unique role for either ADK1 or ADK2, since the removal of either isoform results in decreased ADK activity<br />

but no discernable phenotypic changes. However, reducing overall levels of ADK activity resulted in severe changes<br />

to plant development, <strong>with</strong> lower ADK activity causing more severe phenotypes. Some of the abnormalities associated<br />

<strong>with</strong> the silencing include: decreased DNA methylation, smaller roots, wrinkled leaves, enlarged inflorescent meristems,<br />

clustered inflorescences, delayed leaf and silique senescence and reduced stem development. Secondary shoots that<br />

eventually develop on sADK plants are morphologically similar to those of wild-type Arabidopsis (i.e. contain cauline<br />

leaves and non-clustered inflorescences). We are using ADK-deficient lines generated by overexpression of ADK-GFP<br />

fusion proteins to compare silencing in secondary vs primary shoots. In addition, transformation <strong>with</strong> a constitutively<br />

expressed adenosine deaminase cDNA alleviates the abnormal phenotype of the sADK lines and suggests that increased<br />

adenosine is leading to these traits.

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