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The Arabidopsis thaliana REVOLUTA (REV) protein is a member of the class III homeodomain-leucine zipper (HD-ZIPIII) proteins. REV is a potent regulator of leaf polarity and vascular development. Here, we report the identification of a gene family that encodes small leucine zipper–containing proteins (LITTLE ZIPPER [ZPR] proteins) where the leucine zipper is similar to that found in REV, PHABULOSA, and PHAVOLUTA proteins. The transcript levels of the ZPR genes increase in response to activation of a steroid-inducible REV protein. We show that the ZPR proteins interact with REV in vitro and that ZPR3 prevents DNA binding by REV in vitro. Overexpression of ZPR proteins in Arabidopsis results in phenotypes similar to those seen when HD-ZIPIII function is reduced. We propose a negative feedback model in which REV promotes transcription of the ZPR genes. The ZPR proteins in turn form heterodimers with the REV protein, preventing it from binding DNA. The HD-ZIPIII/ZPR regulatory module would serve not only to dampen the effect of fluctuations in HD-ZIPIII protein levels but more importantly would provide a potential point of regulation (control over the ratio of inactive heterodimers to active homodimers) that could be influenced by other components of the pathway governing leaf polarity.

▪ Abstract Recent progress has been made in the genetic dissection of angiosperm shoot apical meristem (SAM) structure and function. Genes required for proper SAM development have been identified in a variety of species through the isolation of mutants. In addition, genes with expression patterns indicating they play a role in SAM function have been identified molecularly. The processes of SAM formation, self-renewal, and pattern formation within the SAM are examined with an emphasis on the contributions of recent classical and molecular genetic experiments to our understanding of this basic problem in plant developmental biology.

HD-ZIPIII and KANADI transcription factors have opposing and dramatic affects on plant development. Analysis of mutants shows these proteins to be master regulators of ad/abaxial (i.e., upper/lower) leaf polarity, leaf blade outgrowth, and branch formation. Because these factors do their work by regulating other genes, we have focused our attention on defining their targets. We have found overlap between the ad/abaxial regulatory pathway and hormone signaling pathways, especially pathways of abscisic acid and auxin signaling. This has led to the discovery that abscisic acid signaling acts upstream of HD-ZIPIII and KANADI in the control of germination and may ultimately explain how environmental stress pathways control new growth at the shoot apex. Auxin signaling conversely is downstream from HD-ZIPIII and KANADI action with these factors controlling targets at all steps of auxin action-biosynthesis, transport, regulation of transport, and signaling. Based on these findings, we propose a model in which the HD-ZIPIII and KANADI factors pattern auxin response in the embryo. Finally, many genes targeted for control by HD-ZIPIII and KANADI proteins are themselves transcription factors-indicating these master regulators call up tissue specific subprograms of transcriptional control to affect the many polar differences observed across tissues.

The KNOTTED class of plant genes encodes homeodomain proteins. These genes have been found in all plant species where they have been sought and, where examined, show expression patterns that suggest they play an important role in shoot meristem function. Until now, all mutant phenotypes associated with these genes have been due to gain-of-function mutations, making it difficult to deduce their wild-type function. Here we present evidence that the Arabidopsis SHOOT-MERISTEMLESS (STM) gene, required for shoot apical meristem formation during embryogenesis, encodes a class I KNOTTED-like protein. We also describe the expression pattern of this gene in the wild-type plant. To our knowledge, STM is the first gene shown to mark a specific pattern element in the developing plant embryo both phenotypically and molecularly.

The primary shoot apical meristem of Arabidopsis is initiated late in embryogenesis, after the initiation of the cotyledons. We have identified a gene, called SHOOT MERISTEMLESS, which is critical for this process. shoot meristemless mutant seedlings lack a shoot apical meristem but are otherwise healthy and viable. The anatomy of mutant embryos demonstrates that the shoot meristemless-1 mutation completely blocks the initiation of the shoot apical meristem, but has no other obvious effects on embryo development. The failure of shoot meristemless tissue to regenerate shoots in tissue culture suggests that this gene regulates adventitious shoot meristem formation, as well as embryonic shoot meristem formation.

In wild-type Caenorhabditis elegans, the XO male germ line makes only sperm and the XX hermaphrodite germ line makes sperm and then oocytes. In contrast, the germ line of either a male or a hermaphrodite carrying a mutation of the fog-1 (feminization of the germ line) locus is sexually transformed: cells that would normally make sperm differentiate as oocytes. However, the somatic tissues of fog-1 mutants remain unaffected. All fog-1 alleles identified confer the same phenotype. The fog-1 mutations appear to reduce fog-1 function, indicating that the wild-type fog-1 product is required for specification of a germ cell as a spermatocyte. Two lines of evidence indicate that a germ cell is determined for sex at about the same time that it enters meiosis. These include the fog-1 temperature sensitive period, which coincides in each sex with first entry into meiosis, and the phenotype of a fog-1; glp-1 double mutant. Experiments with double mutants show that fog-1 is epistatic to mutations in all other sex-determining genes tested. These results lead to the conclusion that fog-1 acts at the same level as the fem genes at the end of the sex determination pathway to specify germ cells as sperm.

Shoot development is reiterative: shoot apical meristems (SAMs) give rise to branches made of repeating leaf and stem units with new SAMs in turn formed in the axils of the leaves. Thus, new axes of growth are established on preexisting axes. Here we describe the formation of axillary meristems and floral meristems in Arabidopsis by monitoring the expression of the SHOOT MERISTEMLESS and AINTEGUMENTA genes. Expression of these genes is associated with SAMs and organ primordia, respectively. Four stages of axillary meristem development and previously undefined substages of floral meristem development are described. We find parallels between the development of axillary meristems and the development of floral meristems. Although Arabidopsis flowers develop in the apparent absence of a subtending leaf, the expression patterns of AINTEGUMENTA and SHOOT MERISTEMLESS RNAs during flower development suggest the presence of a highly reduced, "cryptic" leaf subtending the flower in Arabidopsis. We hypothesize that the STM-negative region that develops on the flanks of the inflorescence meristem is a bract primordium and that the floral meristem proper develops in the "axil" of this bract primordium. The bract primordium, although initially specified, becomes repressed in its growth.

We designed a study to determine the incidence, cause, and implications of hypoglycemia (or = 2.7 mmol/L, 49 mg/dL) and severe hyperglycemia (or = 22.2 mmol/L, 400 mg/dL) in in-patients at an urban tertiary medical center.A daily computer search of the Laboratory Information System identified all hospitalized patients with hypoglycemia and severe hyperglycemia during a 49-day period. Chart review was used to assess demographic information, risk factors, and epidemiologic variables. The eventual outcome of the hospitalization was obtained by follow-up.The incidence of hypoglycemia was 1.5%, and of hyperglycemia, 1.9%. Seventy-six percent of the hypoglycemic patients and 16% of the hyperglycemic patients had no prior history of diabetes. The mortality rate for hypoglycemic patients was 22.2%; for hyperglycemic patients it was 11.1%. For all other hospitalized patients it was 2.3% (p0.0001). Mortality rates for the black and Hispanic patients who were hypoglycemic (30% and 46%) were significantly higher than for white patients (6%, p0.01).Hypoglycemia and severe hyperglycemia are not uncommon in hospitalized patients and serve as metabolic markers for patients at increased risk for inhospital mortality. Early identification of at-risk patients and the impact of aggressive treatment of their underlying disease processes should be evaluated in future studies.

We have characterized 31 mutations in the gld-1 (defective in germline development) gene of Caenorhabditis elegans. In gld-1 (null) hermaphrodites, oogenesis is abolished and a germline tumor forms where oocyte development would normally occur. By contrast, gld-1 (null) males are unaffected. The hermaphrodite germline tumor appears to derive from germ cells that enter the meiotic pathway normally but then exit pachytene and return to the mitotic cycle. Certain gld-1 partial loss-of-function mutations also abolish oogenesis, but germ cells arrest in pachytene rather than returning to mitosis. Our results indicate that gld-1 is a tumor suppressor gene required for oocyte development. The tumorous phenotype suggests that gld-1(+) may function to negatively regulate proliferation during meiotic prophase and/or act to direct progression through meiotic prophase. We also show that gld-1(+) has an additional nonessential role in germline sex determination: promotion of hermaphrodite spermatogenesis. This function of gld-1 is inferred from a haplo-insufficient phenotype and from the properties of gain-of-function gld-1 mutations that cause alterations in the sexual identity of germ cells.

The flat shape of most leaves enables them to capture sunlight for photosynthesis more efficiently. But how do leaves develop their flat shape? In their Perspective, [McConnell and Barton][1] discuss new work ([ Nath et al ][2].) that reveals how the differential expression of certain genes within developing leaves of the snapdragon makes these leaves flat. [1]: http://www.sciencemag.org/cgi/content/full/299/5611/1328 [2]: http://www.sciencemag.org/cgi/content/short/299/5611/1404

In wild-type Caenorhabditis elegans there are two sexes, self-fertilizing hermaphrodites (XX) and males (XO). To investigate the role of tra-1 in controlling sex determination in germline tissue, we have examined germline phenotypes of nine tra-1 loss-of-function (lf) mutations. Previous work has shown that tra-1 is needed for female somatic development as the nongonadal soma of tra-1(lf) XX mutants is masculinized. In contrast, the germline of tra-1(lf) XX and XO animals is often feminized; a brief period of spermatogenesis is followed by oogenesis, rather than the continuous spermatogenesis observed in wild-type males. In addition, abnormal gonadal (germ line and somatic gonad) phenotypes are observed which may reflect defects in development or function of somatic gonad regulatory cells. Analysis of germline feminization and abnormal gonadal phenotypes of the various mutations alone or in trans to a deficiency reveals that they cannot be ordered in an allelic series and they do not converge to a single phenotypic endpoint. These observations lead to the suggestion that tra-1 may produce multiple products and/or is autoregulated. One interpretation of the germline feminization is that tra-1(+) is necessary for continued specification of spermatogenesis in males. We also report the isolation and characterization of tra-1 gain-of-function (gf) mutations with novel phenotypes. These include temperature sensitive, recessive germline feminization, and partial somatic loss-of-function phenotypes.