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Biology subjects

Lopez, M.

Publications and source records attributed to Lopez, M..

At least 19 recordsLinked to original sources

Identification of Cysteine-Reactive Early Mitotic Inhibitors

Cancer remains a pervasive health problem for millions of Americans, and defining effective anticancer therapeutics remains a major obstacle to the long-term survival of patients. Recent advances in novel chemistries and chemical libraries have enabled researchers to discover and develop covalent inhibitors to treat various diseases, including cancer. This has spurred the generation of cysteine-targeting covalent compound libraries that have not been fully explored within the context of the cell cycle and cell division, which are attractive targets for inhibiting cancer proliferation. We report a novel, cell-based high-content chemical screening strategy for discovering early mitotic spindle assembly inhibitors. We coupled this strategy with a cysteine-reactive covalent compound library containing 3,520 molecules to identify novel early mitotic inhibitors. These inhibitors included a microtubule depolymerizer, a mitotic spindle positioning disruptor, and compounds affecting mitotic spindle structure and chromosome alignment. Two of these compounds triggered mitotic arrest and reduced cell viability at nanomolar concentrations. These inhibitors serve as chemical probes to investigate mechanisms of early cell division and to develop novel cancer therapeutics.

biochemistry↗

An endonuclease V protects Bacillus subtilis against a deaminase toxin and a uracil-containing phage

Bacteria deploy polymorphic toxins to inhibit competitors and rely on cognate immunity proteins to prevent self-intoxication. Immunity determinants act by binding and neutralizing incoming toxins, and in the rare cases where toxin-induced damage is also reversed, that activity resides within the immunity protein itself. Whether a conflict system can instead dedicate a separate gene to repairing the damage is unknown. Here we report that an operon in Bacillus subtilis encodes the toxin YwqJ, its cognate immunity protein YwqK, and EndoV an endonuclease that incises DNA at the lesion the toxin creates. YwqJ is a single-stranded DNA cytidine deaminase translocated by the type VIIb secretion system (T7SSb) to mediate contact-dependent interbacterial antagonism. Unexpectedly, EndoV exhibits a preference for uracil over the canonical hypoxanthine, processing genomic uracil in cells and protecting against YwqJ when immunity is absent. Because EndoV acts on the chemical lesion rather than the effector, its protection is indifferent to the source of deamination. EndoVBs accordingly restricts replication of PBS1, a bacteriophage whose genome naturally substitutes uracil for thymine. These findings establish DNA repair as a novel layer of defense within toxin-immunity loci and reveal a DNA repair mechanism that unifies interbacterial antagonism and antiviral immunity.

microbiology↗

Chromatin remodelling enables enhancer resetting to facilitate the ERK transcriptional response

During development, cellular identity is ultimately determined by transcriptional output: lineage-specific genes must be activated, while genes associated with alternative fates must be repressed. This process depends on the activity of chromatin remodelling complexes, which regulate the accessibility of transcription factors to chromatin regulatory elements. In addition, cellular identity is shaped by exposure to intercellular signals. Understanding the mechanisms by which extracellular signals are translated into changes in the transcriptional program is essential for understanding cell fate decisions during development, as well as in disease conditions such as cancer. Here we describe a rapid and widespread enhancer resetting event in response to ERK signalling in mouse ES cells. This process occurs in two distinct phases: an immediate, genome-wide alteration in transcription factor binding dynamics at regulatory regions which is dependent on the release of paused RNA Polymerase II, followed by the re-establishment of a context appropriate, stable chromatin state. We demonstrate that the chromatin remodelling complex NuRD is required for this reestablishment phase and for the appropriate transcriptional response to ERK signalling. We propose that enhancer resetting places genomic regulatory regions in a state which is permissive to the exchange of transcription factors in order to establish a new, stable enhancer topology enabling rapid yet precise transcriptional response to extracellular signals.

molecular biology↗

LMNA Haploinsufficiency in Human iPSC-Derived Cardiac Organoids Reveals Early Fibrotic Signaling as a Therapeutically Targetable Process

LMNA mutations are a major cause of dilated cardiomyopathy (DCM), with haploinsufficiency representing a common pathogenic mechanism. Yet the earliest disease-initiating events remain poorly defined. Here, we identify a novel intronic splice-site variant, c.937-1G>A, that disrupts pre-mRNA processing and induces nonsense-mediated mRNA decay, resulting in LMNA haploinsufficiency. Using induced pluripotent stem cells (iPSCs) generated from the patients peripheral blood mononuclear cells (PBMCs), we differentiated into self-patterning human cardiac organoids to model early LMNA-DCM in a multicellular human context. Single-nucleus transcriptomics revealed unexpectedly broad remodeling across major cardiac cell types beyond cardiomyocytes. Functionally, LMNA-mutant organoids exhibited impaired contractility, altered calcium handling, and increased arrhythmic activity. These changes were accompanied by early profibrotic activation, including increased reactive oxygen species (ROS), periostin (POSTN) secretion, and CTGF expression. Treatment with the antifibrotic drug nintedanib attenuated this response. Together, these findings show that LMNA haploinsufficiency initiates global pathogenic remodeling at an unexpectedly early developmental stage.

cell biology↗

PVR and Nectin-2 blockade trigger macrophage anti-tumor functions, promote immune cell recruitment and prevent cervical tumor growth.

Despite vaccination, cervical tumors remain a health issue and require treatment improvement. In 2023, Pembrolizumab, an anti-PD-1 immune checkpoint blockade (ICB), was introduced in the case of advanced or metastatic cervical tumors. This treatment significantly increased progression free survival from 20% to 50%. However, some patients remain resistant to anti-PD-1 treatment, which calls for new targets. In our study, we highlighted poliovirus receptor (PVR) and Nectin-2 as potential ICB targets. Indeed, PVR and Nectin-2 are TIGIT ligands, an immunomodulatory checkpoint expressed by regulatory T cells or exhausted T cells. The binding of PVR or Nectin-2 to TIGIT maintains the immunosuppressive signal in the immune cells allowing tumor progression. Furthermore, we observed that PVR and Nectin-2 were highly expressed on tumor cells and tumor associated macrophages (TAMs) accross the different histological subsets of cervical tumors. Therefore, we hypothesized that using anti-PVR and anti-Nectin-2 anti-bodies would lift immunosuppression in cervical tumors. To that end, we used CyTOF to asses precise immunophenotyping of the targets ex vivo, high throughput confocal microscopy to assess phagocytosis, monocyte derived macrophages (MDM) coupled with 3D cell culture models to assess the impact of our treatment on MDM and TAM repolarization and tumor growth. We could demonstrate that our treatment repolarized macrophages towards an inflammatory profile and that this was followed by a reactivation of macrophage cytotoxic function such as phagocytosis. We also demonstrated that anti-PVR and Nectin-2 treatment allowed the control of tumor growth in 2D and 3D cell culture models. We could also develop a pre-clinical model of autologous cell culture from cervical cancer patients. Using the MIVO technology, which combine organotypic culture and fluidics, we could assess peripheral blood mononuclear cells recruitment towards tumor cells in the presence or absence of anti-PVR and anti-Nectin-2. In conclusion we could demonstrate that targeting macrophages via the PVR/Nectin-2 couple reactivates cervical tumor growth control and improves immune cell recruitment.

immunology↗

A hypothalamus-liver-skeletal muscle axis controlled by JNK1 and FGF21 mediates olanzapine-induced insulin resistance in an intraperitoneal treatment in male mice

BackgroundOlanzapine (OLA), a widely prescribed second-generation antipsychotic, is associated with adverse metabolic effects. We recently showed that oral OLA treatment in male mice induces weight gain and hepatic steatosis, whereas intraperitoneal (i.p.) administration leads to weight loss due to higher hypothalamic OLA levels and activation of brown adipose tissue. Since clinical studies report insulin resistance in individuals treated with OLA, here we investigated the impact of OLA i.p. treatment on insulin sensitivity, focusing on the liver- skeletal muscle axis. Material and MethodsWild-type male mice were treated with OLA (10 mg/kg, i.p.) for 8 weeks or received a single intrahypothalamic injection (15 nmol). Glucose homeostasis parameters were assessed. Mechanistic studies were performed in vagotomized mice, mice lacking JNK in either the hypothalamus or liver, mice overexpressing hepatic FGF21, and PTP1B-deficient mice (PTP1B-KO). ResultsOLA i.p. treatment induced systemic insulin resistance, pyruvate intolerance, and reduced insulin signaling in both liver and skeletal muscle. These effects were accompanied by increased hepatic JNK phosphorylation and IRS1 serine phosphorylation. A single intrahypothalamic OLA injection similarly impaired peripheral insulin action and activated hepatic JNK. Deletion of hypothalamic or hepatic JNK1, as well as vagotomy, prevented these defects. OLA reduced hepatic Fgf21 expression, an effect reversed by hypothalamic JNK1 deletion or vagotomy. Hepatic FGF21 overexpression prevented OLA-induced insulin resistance in skeletal muscle but not in liver. PTP1B-KO mice were protected from all metabolic impairments. ConclusionAlthough OLA i.p. treatment prevents weight gain, it decreases peripheral insulin sensitivity through a hypothalamus-liver axis driven by hypothalamic JNK1, which activates hepatic JNK via the vagus nerve, suppresses hepatic FGF21 and ultimately impairs insulin signaling in skeletal muscle. Importantly, the protection conferred by PTP1B deficiency against OLA-induced insulin resistance strongly suggests that targeting PTP1B might prevent metabolic comorbidities in patients under OLA treatment in a personalized manner.

physiology↗

A foundational model for joint sequence-function multi-species modeling at scale for long-range genomic prediction

Genomic prediction and design require models that integrate local sequence features with long-range regulatory dependencies spanning hundreds of kilobases to megabases. Existing approaches have made substantial progress along complementary axes: supervised sequence-to-function models achieve high accuracy for specific assays and organisms, self-supervised genomic foundation models learn transferable representations from large-scale sequence data, and conditional generative models enable principled sequence design guided by functional objectives. However, these strengths are typically realized in isolation--across distinct model classes, architectures, and training regimes--limiting the ability to combine long-context, base-resolution prediction, functional modeling, and controllable generation within a single efficient framework that generalizes across organisms and modalities. Here we introduce Nucleotide Transformer v3 (NTv3), a multi-species foundation model that unifies representation learning, functional-track and genome-annotation prediction, and controllable sequence generation within a common backbone. NTv3 uses a U-Net-like architecture to enable single-base tokenization and efficient modeling of contexts up to 1 Mb. We pre-train NTv3 on 9 trillion base pairs from OpenGenome2 using base-resolution masked language modeling, followed by post-training with a joint objective that integrates continued self-supervision with supervised learning on [~]16,000 functional tracks and annotation labels from 24 animal and plant species. After post-training, NTv3 achieves state-of-the-art accuracy for functional-track prediction and genome annotation across species, outperforming leading sequence-to-function and foundation-model baselines on established benchmarks and on the new NO_SCPLOWTVC_SCPLOW 3 BO_SCPLOWENCHMARKC_SCPLOW, a controlled downstream fine-tuning suite in a standardized 32 kb input / base-resolution output setting. We further show that NTv3 consolidates a shared regulatory grammar across tasks, enabling coherent long-range genome-to-function inference and variant-associated remodeling. Finally, we fine-tune NTv3 into a controllable generative model via masked diffusion language modeling and use it to design enhancer sequences with specified activity levels and promoter selectivity. We validate these designs experimentally, showing that generated enhancers recapitulate the intended activity stratification and achieve the desired promoter-specific activation in cellulo. We release the NTv3 model family together with code and practical cookbooks for long-context training, multispecies post-training, fine-tuning, interpretation, and sequence design.

genomics↗

Neuronal silencing through depolarization block underlies odor discrimination

The olfactory system enables animals to distinguish between attractive and aversive odor sources through the perception of odorant molecules. A fundamental challenge is maintaining stable odor identity perception despite fluctuating stimulus intensities during navigation. Using the numerically simple olfactory system of the Drosophila larva, we combined a quantitative odor discrimination assay, electrophysiology, computational modelling, and ectopic expression of odorant receptors to study the encoding of odor identity. We found that depolarization block, which silences olfactory sensory neurons (OSNs) at odor concentrations 3-4 log units above the detection threshold, enables odor discrimination by creating distinct patterns of OSN activity. In a minimal system with two functional OSNs, larvae discriminate between odors when depolarization block creates differential OSN silencing but fail to distinguish odors producing qualitatively similar activity patterns in both OSNs. This principle extends to odor mixtures and the fully functional olfactory system, where the high affinity of the OR42b odorant receptor for one of the test odors enables discrimination regardless of which OSN expresses OR42b. Our results indicate that depolarization block serves as an integral feature of olfactory coding alongside combinatorial OSN activation. Selective silencing of high-affinity OSNs creates distinct neural representations and enables discrimination between odors that would otherwise produce similar activity patterns. This mechanism appears evolutionarily conserved across sensory systems, from olfactory sensory neurons to photoreceptors, suggesting that selective neuronal silencing serves as a mechanism for maintaining distinct sensory representations across stimulus intensities.

neuroscience↗

Defying expectations: sex-biased telomere dynamics and extended lifespan in the tropical bat species, Molossus molossus.

Telomeres are key biomarkers of cellular ageing, yet their dynamics remain poorly studied in tropical and short-lived bat species. Here, we present the first investigation of telomere length across age in Molossus molossus, a tropical bat historically categorised as the shortest-lived bat on record. Through a multi-year mark-recapture study in Gamboa, Panama, we sampled 492 individuals (n = 317 females, 175 males) and documented a female M. molossus surviving to at least 13 years of age, more than doubling the previously reported maximum lifespan of 5.6 years. Across the population, relative telomere length (rTL) showed no overall significant decline with age. No evidence was found for sex-specific rates of telomere attrition. Rather these results suggest that males and females follow parallel age-related telomere trajectories, with any sex differences primarily reflecting differences in mean telomere length rather than ageing dynamics. Overall, the findings here challenge previous assumptions about the lifespan and ageing biology of M. molossus. They demonstrate that telomere maintenance is not limited to temperate bats, show that sex differences in telomere biology are subtle and species-specific, and reinforce the value of long-term field studies for understanding ageing processes in the wild.

molecular biology↗

Transient let-7/miR-98 reprograms primed pluripotency to induce naivehuman PSCs

Naive human pluripotent stem cells (hPSCs) are valuable for modeling early development and enabling regenerative applications, yet resetting from the primed state remains inefficient and mechanistically unclear. We identify an unexpected role for miR-98-5p, a let-7 family microRNA (miRNA) typically linked to differentiation, in promoting naive induction. Using a synthetic mRNA screen containing diverse miRNA-responsive elements, we uncovered miR-98-5p as a potent enhancer of resetting. Single-cell RNA sequencing and targeted perturbations show that miR-98-5p directly represses NR6A1 while transiently activating BMP2/4 signaling, triggering network transitions. These changes destabilize the primed gene-regulatory network and enable acquisition of a naive state. Leveraging this mechanism, we establish a feeder-free, miRNA-based, editing-free protocol that boosts resetting efficiency from <10% to [~]80%. To our knowledge, this is the first demonstration that a let-7 miRNA can drive naive induction by coupling direct target repression with activation of pro-naive signaling, suggesting a generalizable reprogramming principle of transient network destabilization.

developmental biology↗

TDP-43 expression in the cytoplasm leads to early synaptic and mitochondrial abnormalities in an inducible mouse model of ALS/FTD

TDP-43 proteinopathy is the primary pathology associated with amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), indicating that these neurodegenerative diseases have common underlying mechanisms. We have previously shown that transgenic (Tg) mice conditionally overexpressing a cytoplasmic form of human TDP-43 protein (TDP-43-{Delta}NLS) in forebrain neurons replicate key features of FTD/ALS, including altered cognitive, motor and social behaviors. These behavioral phenotypes and changes in plasticity-related gene expression can be detected as early as 1 month after Tg induction, before overt neurodegeneration occurs. To assess early ultrastructural features in this model, we performed Transmission Electron Microscopy (TEM) analysis in the cortex (Ctx) and hippocampus (Hp) of Tg animals and their non-Tg controls. TEM evaluation of Ctx and Hp revealed that synaptic density was significantly decreased and synapse length was increased in both regions of Tg animals. Synaptic cleft thickness was increased and post-synaptic density thickness was decreased only in the Ctx of Tg mice, revealing differential regional effects in synaptic morphology. We analysed mitochondrial density and we found an increase in the Ctx and a decrease in the Hp of Tg animals, with preserved individual mitochondrial area. Lastly, transcriptomic and proteomic analysis from both transgenic TDP-43-{Delta}NLS mice and human proteinopathy showed widespread decreased expression of synaptic structure and function genes. The alterations in synaptic density and architecture reported here, combined with the mRNA/protein expression data, suggest that TDP-43-{Delta}NLS mice may exhibit abnormal synaptic transmission and that ultrastructural changes play a role in the early behavioral deficits observed in this model. HighlightsO_LICytoplasmic TDP-43 expression in vivo causes early synaptic and mitochondrial abnormalities. C_LIO_LIReduced synaptic density observed in cortical and hippocampal regions of TDP-43-{Delta}NLS mice. C_LIO_LISynaptic ultrastructure altered, including increased cleft width and reduced PSD thickness. C_LIO_LIRegion-specific mitochondrial density changes: increased in cortex, decreased in hippocampus. C_LIO_LIFindings link TDP-43 mislocalization to early structural and functional brain deficits. C_LI

neuroscience↗

CAR T cells targeting Nectin-4 safely overcome resistance to anti-Nectin-4 antibody-drug conjugate in solid tumors

Chimeric antigen receptor T (CAR T) cells represent a promising therapeutic option for a variety of cancers, including solid tumors. Nectin-4 is a cell adhesion molecule expressed at different levels in many solid tumors, including breast and urothelial carcinoma (UC). Enfortumab vedotin (EV), an antibody-drug conjugate (ADC) against Nectin-4, has significantly improved survival in patients with metastatic UC. Skin adverse reactions are frequently observed due to Nectin-4 expression in the epidermis. Here, we developed second-generation CAR T cells against Nectin-4 (N4CART) with a scFv that does not recognize human Nectin-4 expressed in skin keratinocytes. To study the effects of N4CART cell therapy, we used preclinical models of cell-derived xenografts (CDX) and patient-derived xenograft (PDX) of breast cancer expressing moderate to high levels of Nectin-4. We showed a marked efficacy with induction of remissions. Interestingly, N4CART cells kill Nectin-4-positive breast, urothelial and colon tumor cells, which are resistant to EV. Thus, N4CART cells represent a valuable and safe therapy for the treatment of patients with Nectin-4 expressing tumors, including those that are resistant to EV. Finally, baboon-envelope pseudotyped lentiviral vectors (LV) outperformed VSVG-LVs for Nectin-4 CAR expressing in {beta} T cells resulting in an efficient anti-tumoral response in PDX mice.

immunology↗

The chromatin remodeller CHD4 controls both nucleosome integrity and transcription factor binding to promote activity of active regulatory elements and to prevent activation of silent enhancers

Chromatin organisation and transcriptional regulation are tightly coordinated processes that are essential for maintaining cellular identity and function. ATP-dependent chromatin remodelling proteins play critical roles in control of genome structure and in regulating transcription across eukaryotes. Their essential nature, however, has made it difficult to define exactly how these functions are mediated. The chromatin remodeller CHD4 has been shown to be capable of sliding nucleosomes in vitro, and to regulate chromatin accessibility and gene expression in vivo. Using an inducible depletion system, here we identify a second mechanism of action for CHD4 in actively restricting the residence time of transcription factors on chromatin. Together these activities result in distinct, context-dependent outcomes: at highly accessible regulatory elements, CHD4 limits transcription factor binding to maintain regulatory function, while at low-accessibility euchromatic regions, it prevents transcription factor engagement and sustains chromatin compaction, thereby silencing cryptic enhancers. Collectively, these mechanisms enable CHD4 to reduce transcriptional noise while preserving the responsiveness of active regulatory networks.

molecular biology↗

An astrocytic AMPK clock drives circadian behaviour

Circadian clocks coordinate behaviour and physiology with daily cycles of light and nutrient availability, but how metabolic signals influence brain timing remains incompletely understood. Astrocytes integrate metabolic and hormonal cues and exhibit time-of-day-dependent responses, suggesting that they may convey temporal information to hypothalamic circuits. Here, we show that hypothalamic AMP-activated protein kinase (AMPK) exhibits circadian regulation independently of light and feeding cues, is modulated by nutrient availability and astrocytic Ca{superscript 2} signalling, and regulates the temporal organisation of the hypothalamic phosphoproteome. Genetic manipulation of astrocytic AMPK signalling alters PER2 abundance and phosphorylation, including at a conserved residue implicated in circadian period regulation. At the behavioural level, AMPK and PER2 in ventromedial hypothalamic astrocytes contribute to food-anticipatory activity, whereas disruption of astrocytic AMPK signalling alters SCN-dependent circadian locomotor rhythms and energy homeostasis in a sex-dependent manner. Together, these findings identify astrocytic AMPK signalling as a temporally regulated pathway that couples metabolic signals to hypothalamic circadian timing and systemic homeostasis.

neuroscience↗

Sequencing by Expansion (SBX) -- a novel, high-throughput single-molecule sequencing technology

Remarkable advances in high-throughput sequencing have enabled major biological discoveries and clinical applications, but achieving wider distribution and use depends critically on further improvements in scale and cost reduction. Nanopore sequencing has long held the promise for such progress, but has had limited market penetration. This is because efficient and accurate nanopore sequencing of nucleic acids has been challenged by fundamental signal-to-noise limitations resulting from the poor spatial resolution and molecular distinction of nucleobases. Here, we describe Sequencing by Expansion (SBX), a single-molecule sequencing technology that overcomes these limitations by using a biochemical conversion process to encode the sequence of a target nucleic acid molecule into an Xpandomer, a highly measurable surrogate polymer. Expanding over 50 times longer than the parent DNA templates, Xpandomers are engineered with high signal-to-noise reporter codes to enable facile, high-accuracy nanopore sequencing. We demonstrate the performance of SBX and present the specialized molecular structures, chemistries, enzymes and methods that enable it. The innovative molecular and systems engineering in SBX create a transformative technology to address the needs of existing and emerging sequencing applications.

genomics↗

Bioaugmentation in anaerobic digesters: A systematic review

Bioaugmentation, the intentional introduction of specific microorganisms into anaerobic digestion (AD) systems, has shown promise in enhancing methane production and in mitigating stressful conditions, particularly in systems operating below optimal performance. This review presents a systematic literature review (SLR) and meta-analysis to evaluate the efficacy of bioaugmentation strategies in AD. This review identified and analyzed studies meeting predefined eligibility criteria through a structured methodology involving research protocol, search, appraisal, synthesis, analysis, and reporting. A notable innovation of this review is its comprehensive critical comparison of different controls used in bioaugmentation studies, which has been inadequately addressed in previous literature. To facilitate the functional understanding, strains for bioaugmentation were grouped into the four phases of anaerobic digestion (hydrolysis, acidogenesis, acetogenesis and methanogenesis). A highly diverse set of microbes has been described for bioaugmentation, especially from the families Clostridiaceae, Pseudomonadaceae and Syntrophomonadaceae. Most works are related to hydrolysis. The few works that address acidogenesis are mostly related to dark fermentation. Several studies used methanogenic archaea as well as syntrophic acetate oxidising bacteria, despite the difficulties in culturing them. On the other hand, studies applying strains for acetogenesis were largely underrepresented. Especially works on syntrophic propionate and butyrate oxidation (SPO and SBO) were missing.

bioengineering↗

Progressive chromosome shape changes during cell divisions, recapitulated by loop capture simulations

Mitotic chromosomes give genome portions the required compaction and mechanical stability for faithful inheritance during cell divisions. Here, we record human chromosome dimensions from their appearance in prophase over successive times in a mitotic arrest. Chromosomes first appear long and uniformly thin. Then, individual chromosome arms become discernible, which continuously shorten and thicken - the longer a chromosome arm, the thicker it becomes. The observed chromosome arm length to width relationship can be described by a power law with progressively increasing exponent. In the search for a molecular explanation of this behavior, the popular loop extrusion model provides no obvious means by which longer arms become thicker. Instead, we find that simulations of an alternative loop capture model recapitulate key features of our observations, including the gradually developing arm length to width relationship. Our analyses portray chromosomes as out-of-equilibrium structures in the process of transitioning towards, but on biologically relevant time scales not typically reaching, steady state.

biophysics↗

Selecting cacao clones with high productivity potential and tolerance to Black Pod Rot (BPR) and Frosty Pod Rot (FPR).

Cacao (Theobroma cacao) is affected annually by Frosty Pod Rot (FPR) (Moniliopthora roreri) and Black Pod Rot (BPR) (Phytophthora sp). The loss caused by both diseases is threatening cacao production worldwide. Therefore, cacao breeding programs focus on developing new cacao clones with high productivity potential and disease resistance. However, this challenge is not easy to achieve due to the long time required for selection, the influence of environmental conditions on the severity of the disease, and the avoidance of chemical control of diseases. Therefore, genetic resistance should be the best option for selecting and releasing new cacao clones to the farmers. In this study, 40 cacao clones, 20 from CATIE and 20 from FHIA breeding programs were evaluated from 2013 to 2017. Three criteria were used to select clones: Yield, Percentage Disease Pod (PDP), and Disease and Production Index (DPI). Results indicated that depending on the cacao breeding program objectives, it is possible to use those criteria to select new cacao clones that are highly productive and resistant to diseases because cacao clones with high productivity are not always the most resistant to diseases and vice versa; however, a combination of both criteria can be used to select cacao clones with high productivity potential and resistance to FPR and BPR.

pathology↗