Atlas of Science

Day: December 7, 2017

  • Recurrent ontogenesis

    Recurrent ontogenesis

    Flowering plants arose during the Cretaceous, and up to date they count around 235,000 species, representing the largest and most diverse group within the plant kingdom. One of the foundation of their success relies upon the production of the seed, which represent the outstanding solution to conserve the genetic information. In higher plants, during embryogenesis the primary axis of development is established by the shoot apical meristem (SAM) and the root apical meristem (RAM). Throughout plant life apical meristems continually produce new organs (branches, leaves, roots) which are added to those formed during embryogenesis (recurrent ontogenesis). The genetic information is directly delivered from the SAM to the mega- and micro-sporogenous tissues during the reproductive phase. In seed plants, branching, achieved by axillary meristems (AMs), plays a pivotal role in the development of the aboveground plant architecture (Fig. 1).

    Fig. 1. Noteworthy different branching development in Tilia platyphyllos (left) and Washingtonia robusta (right).

    Leaf abaxial (AB) and adaxial (AD) identity appear to be one of the key elements to specify the cell fate for AM initiation in the axil of the leaf base. The network consists mainly of two groups of transcription factors (TFs): the class III HD-ZIP (e.g., PHABULOSA, PHAVOLUTA, REVOLUTA) that promotes AD leaf fate and the YABBY and KANADI (KAN) family that acts antagonistically with HD-ZIP IIIs together with miRNA165/166 to promote AB leaf fate. In addition, KAN proteins directly target genes related to auxin signaling through the AUXIN RESPONSE FACTOR3/ETTIN and ARF4 genes to specify AB fate. Several evidences suggest that the AD domain of a leaf possesses a special competence to form meristems. Class I KNOX family homeodomain TFs together with ARP genes have a key role in regulating the balance between SAM maintenance and organogenesis.

    Fig. 2. Genetic network and hormones [auxin (IAA), gibberellins (GAs), cytokinins (CKs) strigolactones (SLs) and brassinosteroids (BRs)], involved in the control of axillary meristem (AM) initiation in the boundary zone (BZ). Arrows and arrowheads indicate an interaction and/or activation effect; lines with terminal bars indicate a repressive effect. The BZ is indicated with a circle proximal to the insertion of the leaf with the shoot apical meristem. A larger circle is depicted to show hormones and gene product acronyms as well as their interactions in the BZ. AHK/CRE1/WOL: ARABIDOPSIS HISTIDINE KINASE/CR1/WOL; ARR1: ARABIDOPSIS RESPONSE REGULATOR1; BAS1: PHYB ACTIVATION TAGGED SUPPRESSOR1; CUC2/3: CUP-SHAPED COTYLEDON2/3; D14/DAD2: DWARF14/DECREASED APICAL DOMINANCE2; EXB1: EXCESSIVE BRANCHES1; IPT: ISOPENTENYLTRANSFERASE8; LAS: LATERAL SUPPRESSOR; LOB: LATERAL ORGAN BOUNDARIES; miR164A: microRNA164A; RAX: REGULATOR OF AXILLARY MERISTEMS; ROX: REGULATOR OF AXILLARY MERISTEM FORMATION and STM: SHOOTMERISTEMLESS.
    It is well-defined that most genes (e.g., BARREN STALK, CUP-SHAPED COTYLEDON, DECREASED APICAL DOMINANCE, DWARF14, EXCESSIVE BRANCHES1, FASTIGIATE1, LATERAL ORGAN BOUNDARIES, LATERAL ORGAN FUSION 1 and 2, LATERAL SUPPRESSOR, REGULATOR OF AXILLARY MERISTEMS, REGULATOR OF AXILLARY MERISTEM FORMATION) identified through the analysis of mutants with defects in AM and/or floral meristem (FM) initiation, act on limited zones marking the boundary zone (BZ) between the SAM and leaves and/or the BZ between inflorescence/FMs and bracts. These genes have key roles in many aspects of embryo and post-embryo development as well as the establishment of the spatial and temporal regulation of meristematic activity to design the cell fate for AM and FM initiation.

    Mutations that affect the initial steps in reproductive AM formation often result in the development of characteristic pin-like inflorescences, from which the name pin-formed (pin) is derived. Most of the PIN proteins are located in the plasma membrane; they can therefore mediate directional auxin fluxes within tissues and generate auxin maxima and gradients that influence the development of lateral organs. In addition to auxin, the chemical signals required to specify the cell fate for AM initiation in the BZ involve: citokinins (CKs), strigolactones, brassinosteroids, gibberellins and sugar. Therefore, a complex interplay of chemical substances and TFs is established to control AM initiation in the boundary domain (Fig. 2). For example, accurate endogenous auxin and CK levels are sustained by a homeostatic feedback loop in the region of AM initiation. After the establishment of an auxin minimum in the BZ, the activation of CK perception and signaling is required for AM initiation. Therefore, depletion of auxin from leaf axils is a prerequisite for AM formation during vegetative development. Three CK receptors, i.e., ARABIDOPSIS HISTIDINE KINASE2, AHK3, and AHK4/CRE1/WOL, perceive the CK signal to activate the type-B ARABIDOPSIS RESPONSE REGULATOR TFs. Moreover, SHOOT MERISTEMLESS can activate IPT expression to promote CK biosynthesis. These complementary results show the importance of heterogeneous hormone allocation in AM formation.

    Alice Basile 1, Marco Fambrini 2, Claudio Pugliesi 2
    1PlantLab, Sant’Anna School of Advanced Studies, San Giuliano Terme, Pisa, Italy
    2Department of Agriculture, Food and Environment, University of Pisa, Pisa, Italy

     

    Publication

    The vascular plants: open system of growth.
    Basile A, Fambrini M, Pugliesi C
    Dev Genes Evol. 2017 Mar

  • 20th-century version of an old pathogen. Drug resistant tuberculosis

    20th-century version of an old pathogen. Drug resistant tuberculosis

    Mycobacterium tuberculosis the causative agent of human tuberculosis (TB) is consider the most successful pathogen  that could infect (2 billion), induce (10.4 million) and kill (1.7 million) a large number of people around the world. Besides this the rapid evolution of Mycobacterium tuberculosis, from mono-drug-resistant to multiple drug-resistant [MDR-TB; isolates that are resistance to at least isoniazide (INH) and rifampicin (RIF)], extensively drug-resistant [XDR-TB; defined as MDR with additional resistance to both fluoroquinolones and at least one second –line injectable drug], and most recently extremely drug resistant (XXDR) or totally drug-resistant strains (TDR-TB), is threatening to make TB once again an untreatable disease if new therapeutic options do not soon become available.

    Fig. 1. Cross section of cell wall of totally –drug resistant TB bacilli (TDR-TB cell) recorded by atomic force microcopy (AFM).
    The cell wall thickness is clearer with AFM than transmission electron microscopy (TEM). Because the interpreting TEM images need more cautions, since electron microscopy analyses of ultrathin sections are performed with specimens from which water had been removed, consequently, water soluble molecules may aggregate and lipid molecules may be prone to extraction or rearrangement by organic solvents during dehydration. But the cross section using atomic force microscopy performed in water and there is no need of dehydrating the samples. Under AFM, the cell wall thickness reaches 35 ±1.5 nm, almost triple of what usually present in susceptible forms.

    The TDR-TB strains reported to be resistant to ‘all first-line drugs (FLDs) (isoniazid, rifampicin, ethambutol, pyrazinamide, streptomycin) and second-line drugs (SLDs) (fluoroquinolones, ethionamide, amikacin, para-aminosalycilic acid, capreomycin, kanamycin, cycloserine). The first case of TDR- TB was a young Peruvian man who was visiting the United States to study English. His illness originally puzzled the doctors he saw as he had never had TB. Later on in 2007, Migliori et al described the first two cases of XXDR in Italy which were not responding to FLDs, SLDs and other additional drugs (rifabutin, clofazimine, dapsone, claritromycin, thiacetazon). Then, in 2009, Velayati et al reported the first 15 cases of TDR-TB in Iran. The strains were collected from both immigrants (Afghan, 30.4%; Azerbaijani, 8.6%; Iraqi, 4.3%) and Iranian (56.5%) MDR-TB cases. In 2012, India described the isolation of “TDR-TB from Indian patients, and in 2013, Center for Diseases Control and Preventions “reported the TDR-TB cases in South Africa, and they stated that this form of TB diseases was virtually untreatable. Globally, it is estimated that around 10% of all MDR-TB strains are TDR-TB. This number, however, may be not reflecting the correct situation, as many laboratories in endemic TB countries do not have the capacity to detect the XDR or TDR-TB strains. Secondly, surveillance data were available from a very small number of patients in only a few countries, and only those with extensive drug susceptibility testing (DST) capacity.

    Fig. 2. Besides pilli formation; 10- 15% of TDR-TB bacilli develop the outer membrane channels or protrusion tubes that are visible on their cell surface. The function of such channels is remained to be resolve.

    The most terrifying  findings  was when we  demonstrated a marked differences between the  cell wall thickening of XDR and TDR-TB bacilli (up to 35 nm), from  MDR ( 17.1 ±1.3) or susceptible ( 15.6± 1.3nm ) isolates (Fig .1).  This observation raise a debate on the candidate drug(s) that could penetrations inside these isolates? Recently, the light of hope came with effectiveness use of new drugs (bedaquiline and delamanid) or combination of available  drugs (bedaquiline and clofazimine)  to treat DR-TB  patients, but then also more recent investigations showed  MDR-TB isolates had resistant to these drugs also . Additionally, the other adaptive mechanisms like pilli –formation or tubular protrusion were reported in these deadly bacilli (Fig. 2). Thereby, it become clear that we are no more dealing with simple rod shaped Koch bacilli.  Fortunately, the number of these strains (TDR-TB) are very low; but these low number does not permit us to ignore their presence.

    We know that the combination of available drugs might not work-well for these deadly bacilli, but for the time –being we can strictly follow international policy on TB infection control in health-care facilities, congregate settings and households. And maybe we have to revise  the  transmission strategies when we our concern is XDR or TDR-TB bacilli.

    Ali Akbar Velayati, Parissa Farnia
    Mycobacteriology Research Centre (MRC), National Research Institute of Tuberculosis and Lung Disease
    (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran

     

    Publication

    Overview of drug-resistant tuberculosis worldwide.
    Velayati AA, Farnia P, Farahbod AM
    Int J Mycobacteriol. 2016 Dec