Treating Arabidopsis roots with exogenous auxin results in dramatic changes in cellular processes including de novo induction of lateral roots which later emerge through the overlying cells. Microarray experiments reveal approximately 80 genes that are substantially up-regulated in the root over the first 12 h following auxin treatment. We hypothesize that the observed increase in expression of pectate lyase family genes leads to degradation of the pectin-rich middle lamellae, allowing cells in the parent root to separate cleanly. Differences in the degree of pectin methylation in lateral and parent roots may explain why lateral roots are not degraded themselves.

Abstract-Cytoplasmic overexpression of Akt in the heart results in a myopathy characterized by organ and myocyte hypertrophy. Conversely, nuclear-targeted Akt does not lead to cardiac hypertrophy, but the cellular basis of this distinct heart phenotype remains to be determined. Similarly, whether nuclear-targeted Akt affects ventricular performance and mechanics, calcium metabolism, and electrical properties of myocytes is unknown. Moreover, whether the expression and state of phosphorylation of regulatory proteins implicated in calcium cycling and myocyte contractility are altered in nuclear-targeted Akt has not been established. We report that nuclear overexpression of Akt does not modify cardiac size and shape but results in an increased number of cardiomyocytes, which are smaller in volume. Additionally, the heart possesses enhanced systolic and diastolic function, which is paralleled by increased myocyte performance. Myocyte shortening and velocity of shortening and relengthening are increased in transgenic mice and are coupled with a more efficient reuptake of calcium by the sarcoplasmic reticulum (SR). This process increases calcium loading of the SR during relengthening. The enhanced SR function appears to be mediated by an increase in SR Ca 2ϩ -ATPase2a activity sustained by a higher degree of phosphorylation of phospholamban. This posttranslational modification was associated with an increase in phospho-protein kinase A and a decrease in protein phosphatase-1. Together, these observations provide a plausible biochemical mechanism for the potentiation of myocyte and ventricular function in Akt transgenic mice. Therefore, nuclear-targeted Akt in myocytes may have important implications for the diseased heart. Key Words: Akt Ⅲ myocyte mechanics Ⅲ myocyte size and number P rotein kinase B, also referred to as Akt, phosphorylates multiple cytoplasmic and nuclear substrates implicated in cell survival and growth of several organs including the heart. 1 Although myocyte survival and cellular hypertrophy may be viewed as important adaptations of the overloaded heart against the onset of ventricular decompensation, 2 the targeted expression of constitutively activated Akt to the myocardium has resulted in cardiac hypertrophy [3][4][5][6][7] and ventricular dysfunction. 6 In these cases, however, transgene activity was widespread throughout cardiomyocytes at nonphysiological levels, raising the possibility that the nuclear accumulation of Akt may retain the antiapoptotic effects of this serine-threonine kinase, without promoting organ hypertrophy and alterations in cardiac performance. In this regard, hearts of mice expressing nuclear-targeted Akt show no evidence of myopathy 8 in contrast to other cardiac-specific Akt transgenics created with constitutively activated kinase. Targeting of Akt to myocyte nuclei preserves cell viability through the phosphorylation of survival factors within the nucleus that interfere with apoptotic death signaling. 1,8 -11 Thus, whether Akt is expressed in the cytoplasm or in t...

To determine whether stretch-induced activation of p53 is necessary for the up-regulation of the local renin-angiotensin system and angiotensin II (Ang II)-induced apoptosis, ventricular myocytes were infected with an adenoviral vector carrying mutated p53, Adp53m, before 12 hours of stretch. Noninfected myocytes and myocytes infected with AdLacZ served as controls. Stretching of Adp53m-infected myocytes prevented stimulation of p53 function that conditioned the expression of p53-dependent genes; quantity of angiotensinogen (Aogen), AT 1 , and Bax decreased, whereas Bcl-2 increased. Ang II generation was not enhanced by stretch. Conversely, stretch produced opposite changes in noninfected and AdLacZinfected myocytes: Aogen increased twofold, AT 1 increased 2.1-fold, Bax increased 2.5-fold, and Ang II increased 2.4-fold. These responses were coupled with 4.5-fold up-regulation of wild-type p53. Stretch elicited comparable adaptations in p53-independent genes, in the presence or absence of mutated p53; renin increased threefold, angiotensin-converting enzyme increased ninefold, and AT 2 increased 1.7-fold. Infection with Adp53m inhibited myocyte apoptosis after stretch. Conversely, stretch increased apoptosis by 6.2-fold in myocytes with elevated endogenous wild-type p53. Thus, a competitor of p53 function interfered with both stretch-induced Ang II formation and apoptosis, indicating that p53 is a major modulator of myocyte renin-angiotensin system and cell survival after mechanical deformation. The tumor suppressor gene, p53, has been implicated in the modulation of cardiac myocyte apoptosis in vitro

It is widely held that injured neurons in the central nervous system do not undergo axonal regrowth. However, there is mounting evidence that serotonin axons are a notable exception. Serotonin axons undergo long-distance regrowth in the neocortex after amphetamine lesion and, following a penetrating stab injury, they can regrow from cut ends to traverse the stab rift. Traumatic brain injury (TBI) is clinically prevalent and can lead to pathologies such as depression that are related to serotonergic dysfunction. Thus, whether serotonin axons can regrow after TBI is an important question. We used two models for TBI, a persistent open skull condition and controlled cortical impact, to evoke injury in adult female mouse neocortex and assessed serotonin axon density one week, one month, and three months after injury by serotonin transporter immunohistochemistry. We found that following both forms of TBI, serotonin axon density is decreased posterior but not anterior to the injury site when measured in layer 1 at one week post-surgery, and that serotonin axons are capable of regrowing into the distal zone to increase density by one month post-surgery. This pattern is consistent with the anterior-to-posterior course of serotonin axons in the neocortex. TBI in these models is associated with significant reactive astrogliosis both anterior and posterior to the impact, but the degree of reactive astrogliosis is not correlated with serotonin axon density when measured one week after TBI. Microglial density remains constant following both types of injuries, but microglial condensation was detected one week after controlled cortical impact.